metadata: run_metadata: 272 rows where experiment.library_layout = "PAIRED", technology = "unknown" and tissue

272 rows where experiment.library_layout = "PAIRED", technology = "unknown" and tissue_curation = "Cancer or Tumor"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	study.attributes	study.PMIDs	sample.title	sample.alias	sample.attributes	GEOsample.title	GEOsample.dataprocessing	GEOsample.source	GEOsample.treatmentprotocol	GEOsample.extractprotocol	GEOsample.growthprotocol	GEOsample.characteristics	GEOsample.accession	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_construction_protocol	experiment.attributes	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.Ncount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.n_mates	seqdetective.mapping_rate.mate1	seqdetective.mapping_rate.mate2	seqdetective.nofeature_rate.mate1	seqdetective.nofeature_rate.mate2	seqdetective.sparsity.mate1	seqdetective.sparsity.mate2	seqdetective.pos_strand_rate.mate1	seqdetective.pos_strand_rate.mate2	seqdetective.readlen.mate1	seqdetective.readlen.mate2	seqdetective.judgement.mate1	seqdetective.judgement.mate2	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
34353	34353	SRR31668404	SRX27031101	SRS23495066	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven tp53 / primary neuroblastoma biological sample 3	GSM8675202	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven tp53 / primary neuroblastoma biological sample 3	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 /	GSM8675202	GSM8675202: MYCN driven tp53 / primary neuroblastoma biological sample 3; Danio rerio; RNA Seq	GSM8675202 r1	GSM8675202	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	tp53_3_R1.fastq.gz tp53_3_R2.fastq.gz	fastq fastq	23336192320.0	77272160.0	GSM8675202 r1	0:151 1:151	A:6254847499;C:5434444966;G:5467895678;T:6178911394;N:92783	151	151	6254847499	5434444966	5467895678	6178911394	92783	SRX27031101	SRS23495066	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34354	34354	SRR31668405	SRX27031100	SRS23495065	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven tp53 / primary neuroblastoma biological sample 2	GSM8675201	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven tp53 / primary neuroblastoma biological sample 2	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 /	GSM8675201	GSM8675201: MYCN driven tp53 / primary neuroblastoma biological sample 2; Danio rerio; RNA Seq	GSM8675201 r1	GSM8675201	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	tp53_2_R1.fastq.gz tp53_2_R2.fastq.gz	fastq fastq	20339315252.0	67348726.0	GSM8675201 r1	0:151 1:151	A:5418776023;C:4755013552;G:4799958409;T:5365490819;N:76449	151	151	5418776023	4755013552	4799958409	5365490819	76449	SRX27031100	SRS23495065	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34355	34355	SRR31668406	SRX27031099	SRS23495064	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven tp53 / primary neuroblastoma biological sample 1	GSM8675200	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven tp53 / primary neuroblastoma biological sample 1	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;tp53 /	GSM8675200	GSM8675200: MYCN driven tp53 / primary neuroblastoma biological sample 1; Danio rerio; RNA Seq	GSM8675200 r1	GSM8675200	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	tp53_1_R1.fastq.gz tp53_1_R2.fastq.gz	fastq fastq	23005026972.0	76175586.0	GSM8675200 r1	0:151 1:151	A:6117051407;C:5407786944;G:5434080472;T:6046021055;N:87094	151	151	6117051407	5407786944	5434080472	6046021055	87094	SRX27031099	SRS23495064	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34356	34356	SRR31668407	SRX27031098	SRS23495063	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven atm+/ ;tp53+/ primary neuroblastoma	GSM8675199	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;atm+/ ;tp53+/ \|geo loc name:missing\|collection date:missing	MYCN driven atm+/ ;tp53+/ primary neuroblastoma	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;atm+/ ;tp53+/	GSM8675199	GSM8675199: MYCN driven atm+/ ;tp53+/ primary neuroblastoma; Danio rerio; RNA Seq	GSM8675199 r1	GSM8675199	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	atm_2_R1.fastq.gz atm_2_R2.fastq.gz	fastq fastq	23261284240.0	77024120.0	GSM8675199 r1	0:151 1:151	A:6145376247;C:5458254950;G:5636744711;T:6020701748;N:206584	151	151	6145376247	5458254950	5636744711	6020701748	206584	SRX27031098	SRS23495063	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34357	34357	SRR31668408	SRX27031097	SRS23495062	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven atm+/ ;tp53 / primary neuroblastoma	GSM8675198	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;atm+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven atm+/ ;tp53 / primary neuroblastoma	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;atm+/ ;tp53 /	GSM8675198	GSM8675198: MYCN driven atm+/ ;tp53 / primary neuroblastoma; Danio rerio; RNA Seq	GSM8675198 r1	GSM8675198	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	atm_1_R1.fastq.gz atm_1_R2.fastq.gz	fastq fastq	28077605910.0	92972205.0	GSM8675198 r1	0:151 1:151	A:7498074413;C:6502104689;G:6709307820;T:7367870925;N:248063	151	151	7498074413	6502104689	6709307820	7367870925	248063	SRX27031097	SRS23495062	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34358	34358	SRR31668409	SRX27031096	SRS23495061	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 3	GSM8675197	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 3	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675197	GSM8675197: MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 3; Danio rerio; RNA Seq	GSM8675197 r1	GSM8675197	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_4T_3_R1.fastq.gz brca2_4T_3_R2.fastq.gz	fastq fastq	25734256842.0	85212771.0	GSM8675197 r1	0:151 1:151	A:6992891847;C:5899631235;G:5926941082;T:6914693910;N:98768	151	151	6992891847	5899631235	5926941082	6914693910	98768	SRX27031096	SRS23495061	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34359	34359	SRR31668410	SRX27031095	SRS23495060	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 2	GSM8675196	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 2	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675196	GSM8675196: MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 2; Danio rerio; RNA Seq	GSM8675196 r1	GSM8675196	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_4T_2_R1.fastq.gz brca2_4T_2_R2.fastq.gz	fastq fastq	25491325626.0	84408363.0	GSM8675196 r1	0:151 1:151	A:6895400993;C:5873291336;G:5902861384;T:6819673005;N:98908	151	151	6895400993	5873291336	5902861384	6819673005	98908	SRX27031095	SRS23495060	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34360	34360	SRR31668411	SRX27031094	SRS23495059	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 1	GSM8675195	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 1	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675195	GSM8675195: MYCN driven brca2+/ ;tp53 / primary neuroblastoma 4x serially passaged by transplant biological sample 1; Danio rerio; RNA Seq	GSM8675195 r1	GSM8675195	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_4T_1_R1.fastq.gz brca2_4T_1_R2.fastq.gz	fastq fastq	31806877070.0	105320785.0	GSM8675195 r1	0:151 1:151	A:8688753401;C:7248230638;G:7264489119;T:8605282978;N:120934	151	151	8688753401	7248230638	7264489119	8605282978	120934	SRX27031094	SRS23495059	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34361	34361	SRR31668412	SRX27031093	SRS23495058	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 3	GSM8675194	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 3	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675194	GSM8675194: MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 3; Danio rerio; RNA Seq	GSM8675194 r1	GSM8675194	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_3_R1.fastq.gz brca2_3_R2.fastq.gz	fastq fastq	24462829594.0	81002747.0	GSM8675194 r1	0:151 1:151	A:6540455142;C:5666171087;G:5856369054;T:6399621980;N:212331	151	151	6540455142	5666171087	5856369054	6399621980	212331	SRX27031093	SRS23495058	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34362	34362	SRR31668413	SRX27031092	SRS23495057	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 2	GSM8675193	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 2	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675193	GSM8675193: MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 2; Danio rerio; RNA Seq	GSM8675193 r1	GSM8675193	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_2_R1.fastq.gz brca2_2_R2.fastq.gz	fastq fastq	28830972694.0	95466797.0	GSM8675193 r1	0:151 1:151	A:7699874582;C:6741660506;G:6766796779;T:7622528008;N:112819	151	151	7699874582	6741660506	6766796779	7622528008	112819	SRX27031092	SRS23495057	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
34363	34363	SRR31668414	SRX27031091	SRS23495056	SRP550584	PRJNA1196438	DNA Damage Response Deficiency Enhances Neuroblastoma Progression and Sensitivity to Combination PARP and ATR Inhibition	GSE283976	Transcriptome Analysis	Next generation sequencing of neuroblastoma NB tumors have revealed frequent somatic and germline genetic alterations in genes encoding proteins involved in DNA damage response DDR pathways. Despite being well studied in many adult cancers roles for DDR disruption in pediatric solid tumors have not been fully elucidated. To address this patient relevant loss of function mutations in DDR pathway components including Brca2 Atm and Palb2 were incorporated into an established zebrafish MYCN transgenic model Tgdbh:EGFP MYCN. These mutations were found to enhance NB formation and metastasis in vivo and result in upregulation of proliferation cell cycle checkpoint and DNA damage repair transcriptional signatures revealing novel molecular vulnerabilities in DDR deficient NB. Zebrafish DDR deficient NB and human NB cells with DDR protein knock down were sensitive to the polyADP ribose polymerase PARP inhibitor olaparib and this effect was further enhanced by inhibition of the ataxia telangiectasia and rad3 related ATR kinase. Altogether our data supports a functional role for DDR deficiency in NB in vivo and therapeutic potential for combination PARP + ATR inhibition in NB patients with alterations in DDR genes. Overall design: To capture broad transcriptomic differences associated with HDR/DDR deficiency in primary and transplanted neuroblastoma we performed RNA sequencing of GFP+ sorted tumor cells from zebrafish MYCN driven neuroblastoma from various engineered genetic backgrounds			MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 1	GSM8675192	source name:GFP+ sorted neuroblastoma\|tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 / \|geo loc name:missing\|collection date:missing	MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 1	Raw .fastq data was processed using Salmon quantification of transcripts. A “decoy aware” index was built with the Danio rerio transcriptome and genome using the GRCz11 assembly with a k mers length of 23. Samples were quantified with the following arguments: r seqBias mp 3 validateMappings rangeFactorizationBins 4. Assembly: GRCz11 Supplementary files format and content: Comma separated values .csv file including raw non normalized counts for all conditions generated by Salmon	GFP+ sorted neuroblastoma	All animal monitoring and sample collection were performed in accordance with animal use protocols approved by the Hospital for Sick Children Animal Care Committee #1000054111 #1000064586.	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.	Zebrafish were reared and maintained according to standard husbandry procedure at the Zebrafish Genetics and Disease Modeling Core Facility at the Hospital for Sick Children.	tissue:GFP+ sorted neuroblastoma\|cell type:neuroblastoma\|genotype:MYCN;brca2+/ ;tp53 /	GSM8675192	GSM8675192: MYCN driven brca2+/ ;tp53 / primary neuroblastoma biological sample 1; Danio rerio; RNA Seq	GSM8675192 r1	GSM8675192	1	Dissected neuroblastoma tumors were manually dissociated and processed to single cell suspensions. GFP+ tumor cells were sorted from bulk tissue at the SickKids UHN Flow Cytometry Core Facility on a Sony MA900 VBYR cell sorter before pelleting and lysis using Qiagen RNeasy Mini Kit as per manufacturer instructions. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760. Sequence ready polyA enriched libraries were prepared using the NEB Ultra II Directional mRNA prep kit for Illumina NEB E7760.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq X	SRP550584	brca2_1_R1.fastq.gz brca2_1_R2.fastq.gz	fastq fastq	24936530788.0	82571294.0	GSM8675192 r1	0:151 1:151	A:6625695379;C:5867258006;G:5887073244;T:6556406745;N:97414	151	151	6625695379	5867258006	5887073244	6556406745	97414	SRX27031091	SRS23495056	SRA2031529	Hayes Lab, DSCB, Sickkids Research	Hayes Lab, DSCB, Sickkids Research												B	B	biological fallback assumption	illumina	novaseq_era	unknown	poly_a	unknown	bulk	unknown	unknown	Canada	2024-12-10	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
40456	40456	SRR3169301	SRX1584902	SRS1302559	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:SATB2 tumor 3	GSM2061399	source name:SATB2 3\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:SATB2 tumor 3	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	SATB2 3	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061399	GSM2061399: MCR:SATB2 tumor 3; Danio rerio; RNA Seq	GSM2061399		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061399	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-7_R2.fastq.gz EvR-7_R1.fastq.gz	fastq fastq	9597529848.0	47512524.0	GSM2061399 r1	0:101 1:101	A:2382410076;C:2407580203;G:2401045751;T:2403277437;N:3216381	101	101	2382410076	2407580203	2401045751	2403277437	3216381	SRX1584902	SRS1302559	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.91036	0.90143	0.35231	0.35333	0.73701	0.74464	0.54407	0.55412	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
40457	40457	SRR3169300	SRX1584901	SRS1302560	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:SATB2 tumor 2	GSM2061398	source name:SATB2 2\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:SATB2 tumor 2	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	SATB2 2	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061398	GSM2061398: MCR:SATB2 tumor 2; Danio rerio; RNA Seq	GSM2061398		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061398	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-6_R1.fastq.gz EvR-6_R2.fastq.gz	fastq fastq	8239248720.0	40788360.0	GSM2061398 r1	0:101 1:101	A:2050158124;C:2039805258;G:2055117618;T:2091456014;N:2711706	101	101	2050158124	2039805258	2055117618	2091456014	2711706	SRX1584901	SRS1302560	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.89794	0.89327	0.4125	0.40937	0.74	0.74598	0.49301	0.51668	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
40458	40458	SRR3169299	SRX1584900	SRS1302561	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:SATB2 tumor 1	GSM2061397	source name:SATB2 1\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:SATB2 tumor 1	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	SATB2 1	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061397	GSM2061397: MCR:SATB2 tumor 1; Danio rerio; RNA Seq	GSM2061397		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061397	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-5_R1.fastq.gz EvR-5_R2.fastq.gz	fastq fastq	9154990470.0	45321735.0	GSM2061397 r1	0:101 1:101	A:2196552266;C:2343147947;G:2363804516;T:2248519959;N:2965782	101	101	2196552266	2343147947	2363804516	2248519959	2965782	SRX1584900	SRS1302561	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.93607	0.93161	0.24224	0.23511	0.75343	0.7587	0.50166	0.50302	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
40459	40459	SRR3169298	SRX1584899	SRS1302562	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:EGFP tumor 3	GSM2061396	source name:EGFP 3\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:EGFP tumor 3	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	EGFP 3	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061396	GSM2061396: MCR:EGFP tumor 3; Danio rerio; RNA Seq	GSM2061396		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061396	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-3_R2.fastq.gz EvR-3_R1.fastq.gz	fastq fastq	8307858828.0	41128014.0	GSM2061396 r1	0:101 1:101	A:2148512897;C:1987958154;G:2004557741;T:2164084488;N:2745548	101	101	2148512897	1987958154	2004557741	2164084488	2745548	SRX1584899	SRS1302562	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.89808	0.88969	0.36112	0.35518	0.719	0.72711	0.50262	0.49961	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
40460	40460	SRR3169297	SRX1584898	SRS1302563	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:EGFP tumor 2	GSM2061395	source name:EGFP 2\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:EGFP tumor 2	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	EGFP 2	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061395	GSM2061395: MCR:EGFP tumor 2; Danio rerio; RNA Seq	GSM2061395		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061395	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-2_R2.fastq.gz EvR-2_R1.fastq.gz	fastq fastq	7890162016.0	39060208.0	GSM2061395 r1	0:101 1:101	A:2172564285;C:1760424902;G:1758426718;T:2196099270;N:2646841	101	101	2172564285	1760424902	1758426718	2196099270	2646841	SRX1584898	SRS1302563	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.89676	0.89022	0.35914	0.35869	0.72748	0.73328	0.50126	0.48386	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
40461	40461	SRR3169296	SRX1584897	SRS1302564	SRP070127	PRJNA312107	SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA Seq]	GSE77922	Transcriptome Analysis	We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP. Overall design: RNA seq was performed on three biological replicates of primary zebrafish melanoma tumors that were excized from MCR:EGFP control and MCR:SATB2 overexpressing TgBRAF V600E;p53 / ; mitf / zebrafish.	parent bioproject:PRJNA312106		MCR:EGFP tumor 1	GSM2061394	source name:EGFP 1\|tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	MCR:EGFP tumor 1	Quality control of RNA Seq datasets was performed by FastQC18 and Cutadapt19 to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer7 of zebrafish genome using Tophat20 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks21 2.2.1. FPKM values were used to normalize and quantify each transcript. Genome build: Danio rerio UCSC danRer7 Supplementary files format and content: tab delimited text file containg the FPKM value of each gene	EGFP 1	Zebrafish Tgmitfa:BRAFV600E; p53 / ; mitfa / one cell stage embryos were injected with a MiniCoopR expression vector to induce melanocyte specific overexpression of either EGFP control or human SATB2 raised to maturity and monitored for melanoma formation.	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol		tissue:primary melanoma tumor\|genotype:Tgmitfa:BRAFV600E; p53 / ; mitfa /	GSM2061394	GSM2061394: MCR:EGFP tumor 1; Danio rerio; RNA Seq	GSM2061394		1	Zebrafish melanomas were isolated and mechanically homogenized in RTL buffer Qiagen containing β mercaptoethanol. Tumor lysates were transferred onto a QiaShredder column Qiagen and RNA isolation was performed using the RNA Micro Plus kit Qiagen according to the manufacturers instruction. Total RNA was depleted of ribosomal RNA with the Ribo Zero Gold kit Epicentre. Ribosome depleted RNA was used to create multiplexed RNA seq libraries NEBNext Ultra according to manufacturer's protocol	GEO Accession:GSM2061394	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP070127	EvR-1_R2.fastq.gz EvR-1_R1.fastq.gz	fastq fastq	8226747950.0	40726475.0	GSM2061394 r1	0:101 1:101	A:1937216496;C:2135232355;G:2150394263;T:2001262497;N:2642339	101	101	1937216496	2135232355	2150394263	2001262497	2642339	SRX1584897	SRS1302564	SRA353730	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.94058	0.93759	0.26678	0.26414	0.77277	0.77648	0.4952	0.49739	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2016-02-15	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
41084	41084	SRR3666784	SRX1845189	SRS1504028	SRP076552	PRJNA325656	Differential gene expression of zebrafish melanocytes and melanomas [RNA seq]	GSE83343	Transcriptome Analysis	We report the gene expression comparison of zebrafish melanocytes and melanomas. These comparisons were used for integrative genomic studies that identified the BMP factor GDF6 as a new oncogene that is specifically expressed in melanomas. Overall design: Examination of gene expression in two different cell types	parent bioproject:PRJNA325808	pubmed:29202482	ZF melanoma rep4	GSM2199909	tissue:melanoma\|strain:Tgmitfa:BRAFV600E; p53zdf1; Tgmitfa:EGFP; albb4\|age:adult\|cell type:melanoma	ZF melanoma rep4	Star v2.3 was used to align the reads htseq count was used to count mappped reads DESeq2 was used to perform differential gene expression analysis Genome build: Zebrafish Zv9 Supplementary files format and content: tab delimited txt file includes FPKM values for all samples	melanoma		RNA was harvested from cells using Trizol reagent. Illumina TruSeq	Unpigmented EGFP positive melanocytes and melanoma cells were isolated by FACS	strain:Tgmitfa:BRAFV600E;p53zdf1;Tgmitfa:EGFP;albb4\|age:adult\|cell type:melanoma	GSM2199909	GSM2199909: ZF melanoma rep4; Danio rerio; RNA Seq	GSM2199909		1	RNA was harvested from cells using Trizol reagent. Illumina TruSeq	GEO Accession:GSM2199909	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP076552	Melanoma_4_R1.fastq.gz Melanoma_4_R2.fastq.gz	fastq fastq	5824407060.0	57102030.0	GSM2199909 r1	0:51 1:51	A:1623471404;C:1272539670;G:1281078941;T:1643101126;N:4215919	51	51	1623471404	1272539670	1281078941	1643101126	4215919	SRX1845189	SRS1504028	SRA433946	GEO	PMM Bioinformatics Core, Program in Molecular Medicine, University of Massachusetts	2	0.9269	0.87875	0.16101	0.15437	0.75601	0.76479	0.52959	0.49449	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2016-06-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
41085	41085	SRR3666783	SRX1845188	SRS1504029	SRP076552	PRJNA325656	Differential gene expression of zebrafish melanocytes and melanomas [RNA seq]	GSE83343	Transcriptome Analysis	We report the gene expression comparison of zebrafish melanocytes and melanomas. These comparisons were used for integrative genomic studies that identified the BMP factor GDF6 as a new oncogene that is specifically expressed in melanomas. Overall design: Examination of gene expression in two different cell types	parent bioproject:PRJNA325808	pubmed:29202482	ZF melanoma rep3	GSM2199908	tissue:melanoma\|strain:Tgmitfa:BRAFV600E; p53zdf1; Tgmitfa:EGFP; albb4\|age:adult\|cell type:melanoma	ZF melanoma rep3	Star v2.3 was used to align the reads htseq count was used to count mappped reads DESeq2 was used to perform differential gene expression analysis Genome build: Zebrafish Zv9 Supplementary files format and content: tab delimited txt file includes FPKM values for all samples	melanoma		RNA was harvested from cells using Trizol reagent. Illumina TruSeq	Unpigmented EGFP positive melanocytes and melanoma cells were isolated by FACS	strain:Tgmitfa:BRAFV600E;p53zdf1;Tgmitfa:EGFP;albb4\|age:adult\|cell type:melanoma	GSM2199908	GSM2199908: ZF melanoma rep3; Danio rerio; RNA Seq	GSM2199908		1	RNA was harvested from cells using Trizol reagent. Illumina TruSeq	GEO Accession:GSM2199908	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP076552	Melanoma_3_R1.fastq.gz Melanoma_3_R2.fastq.gz	fastq fastq	6025625112.0	59074756.0	GSM2199908 r1	0:51 1:51	A:1664666728;C:1334918212;G:1342599896;T:1679035262;N:4405014	51	51	1664666728	1334918212	1342599896	1679035262	4405014	SRX1845188	SRS1504029	SRA433946	GEO	PMM Bioinformatics Core, Program in Molecular Medicine, University of Massachusetts	2	0.93254	0.8901	0.13621	0.13127	0.75858	0.76562	0.52486	0.51808	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2016-06-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
41086	41086	SRR3666782	SRX1845187	SRS1504027	SRP076552	PRJNA325656	Differential gene expression of zebrafish melanocytes and melanomas [RNA seq]	GSE83343	Transcriptome Analysis	We report the gene expression comparison of zebrafish melanocytes and melanomas. These comparisons were used for integrative genomic studies that identified the BMP factor GDF6 as a new oncogene that is specifically expressed in melanomas. Overall design: Examination of gene expression in two different cell types	parent bioproject:PRJNA325808	pubmed:29202482	ZF melanoma rep2	GSM2199907	tissue:melanoma\|strain:Tgmitfa:BRAFV600E; p53zdf1; Tgmitfa:EGFP; albb4\|age:adult\|cell type:melanoma	ZF melanoma rep2	Star v2.3 was used to align the reads htseq count was used to count mappped reads DESeq2 was used to perform differential gene expression analysis Genome build: Zebrafish Zv9 Supplementary files format and content: tab delimited txt file includes FPKM values for all samples	melanoma		RNA was harvested from cells using Trizol reagent. Illumina TruSeq	Unpigmented EGFP positive melanocytes and melanoma cells were isolated by FACS	strain:Tgmitfa:BRAFV600E;p53zdf1;Tgmitfa:EGFP;albb4\|age:adult\|cell type:melanoma	GSM2199907	GSM2199907: ZF melanoma rep2; Danio rerio; RNA Seq	GSM2199907		1	RNA was harvested from cells using Trizol reagent. Illumina TruSeq	GEO Accession:GSM2199907	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP076552	Melanoma_2_R1.fastq.gz Melanoma_2_R2.fastq.gz	fastq fastq	5820855420.0	57067210.0	GSM2199907 r1	0:51 1:51	A:1608054488;C:1286088047;G:1295801092;T:1626675668;N:4236125	51	51	1608054488	1286088047	1295801092	1626675668	4236125	SRX1845187	SRS1504027	SRA433946	GEO	PMM Bioinformatics Core, Program in Molecular Medicine, University of Massachusetts	2	0.9408	0.88645	0.14414	0.13333	0.76441	0.77291	0.53482	0.53362	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2016-06-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
41087	41087	SRR3666780	SRX1845186	SRS1504026	SRP076552	PRJNA325656	Differential gene expression of zebrafish melanocytes and melanomas [RNA seq]	GSE83343	Transcriptome Analysis	We report the gene expression comparison of zebrafish melanocytes and melanomas. These comparisons were used for integrative genomic studies that identified the BMP factor GDF6 as a new oncogene that is specifically expressed in melanomas. Overall design: Examination of gene expression in two different cell types	parent bioproject:PRJNA325808	pubmed:29202482	ZF melanoma rep1	GSM2199906	tissue:melanoma\|strain:Tgmitfa:BRAFV600E; p53zdf1; Tgmitfa:EGFP; albb4\|age:adult\|cell type:melanoma	ZF melanoma rep1	Star v2.3 was used to align the reads htseq count was used to count mappped reads DESeq2 was used to perform differential gene expression analysis Genome build: Zebrafish Zv9 Supplementary files format and content: tab delimited txt file includes FPKM values for all samples	melanoma		RNA was harvested from cells using Trizol reagent. Illumina TruSeq	Unpigmented EGFP positive melanocytes and melanoma cells were isolated by FACS	strain:Tgmitfa:BRAFV600E;p53zdf1;Tgmitfa:EGFP;albb4\|age:adult\|cell type:melanoma	GSM2199906	GSM2199906: ZF melanoma rep1; Danio rerio; RNA Seq	GSM2199906		1	RNA was harvested from cells using Trizol reagent. Illumina TruSeq	GEO Accession:GSM2199906	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP076552	Melanoma_1_R1.fastq.gz Melanoma_1_R2.fastq.gz	fastq fastq	6005883522.0	58881211.0	GSM2199906 r1	0:51 1:51	A:1674714880;C:1311907155;G:1323946262;T:1691018505;N:4296720	51	51	1674714880	1311907155	1323946262	1691018505	4296720	SRX1845186	SRS1504026	SRA433946	GEO	PMM Bioinformatics Core, Program in Molecular Medicine, University of Massachusetts	2	0.9244	0.87204	0.16657	0.15895	0.74921	0.75688	0.52057	0.51652	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2016-06-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
41570	41570	SRR5044686	SRX2367696	SRS1813795	SRP093723	PRJNA354577	RNA seq of zebrafish melanoma cells post metastatic dissemination	GSE90143	Transcriptome Analysis	We report how the zebrafish melanoma cell line ZMEL1 changes post intravascular injection into 2dpf zebrafish embryos as compared to the cells growing in vitro. Overall design: Examination of ZMEL1 cells in vitro versus 21 days in vivo in the zebrafish		pubmed:28181494	ZMEL1 METASTATIC REP 1	GSM2399710	tissue:ZMEL1 cells in vivo\|cell type:ZMEL1\|tissue type:melanoma	ZMEL1 METASTATIC REP 1	GSNAP alignment to Av9 zebrafish reference genome Read counts extracted with HTSeq Differential expression with DeSeq2 Zebrafish genes converted to human orthologs using DIOPT Genome build: Zv9 Supplementary files format and content: XLSX sheet with normalized read counts output from HTSeq	ZMEL1 cells in vivo	n/a	Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq	in vitro: DMEM/10% FCS/1X glutamax/28.5C in vivo: growth in the zebrafish from 2 21dpf	cell type:ZMEL1\|tissue type:melanoma	GSM2399710	GSM2399710: ZMEL1 METASTATIC REP 1; Danio rerio; RNA Seq	GSM2399710		1	Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq	GEO Accession:GSM2399710	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP093723	DISSEMINATED-1-GFP-POS_GGCTAC_AC62F2ANXX_L006_001.R1.fastq DISSEMINATED-1-GFP-POS_GGCTAC_AC62F2ANXX_L006_001.R2.fastq	fastq fastq	1056705000.0	10567050.0	GSM2399710 r1	0:50 1:50	A:276214070;C:230055594;G:254656322;T:295743831;N:35183	50	50	276214070	230055594	254656322	295743831	35183	SRX2367696	SRS1813795	SRA497524	GEO	White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center	2	0.87206	0.87707	0.36	0.36551	0.80661	0.81442	0.67855	0.54025	50	50	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2016-11-22	Larval	Larval	Cancer or Tumor	Cancer or Tumor
42480	42480	SRR5639268	SRX2877668	SRS2249441	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 8	GSM2646589	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 8	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646589	GSM2646589: MYC 8; Danio rerio; RNA Seq	GSM2646589		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646589	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-8_MWZ3676_S8_R1_001.fastq.gz 20161116_MYC-8_MWZ3676_S8_R2_001.fastq.gz	fastq fastq	10081869900.0	67212466.0	GSM2646589 r1	0:75 1:75	A:2790689900;C:2299822096;G:2324357632;T:2662657984;N:4342288	75	75	2790689900	2299822096	2324357632	2662657984	4342288	SRX2877668	SRS2249441	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.90216	0.90346	0.05109	0.05044	0.75073	0.75552	0.53113	0.44417	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42481	42481	SRR5639267	SRX2877667	SRS2249444	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 7	GSM2646588	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 7	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646588	GSM2646588: MYC 7; Danio rerio; RNA Seq	GSM2646588		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646588	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-7_MWZ3676_S7_R1_001.fastq.gz 20161116_MYC-7_MWZ3676_S7_R2_001.fastq.gz	fastq fastq	9707643300.0	64717622.0	GSM2646588 r1	0:75 1:75	A:2656490466;C:2245711917;G:2271269818;T:2529962783;N:4208316	75	75	2656490466	2245711917	2271269818	2529962783	4208316	SRX2877667	SRS2249444	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.89705	0.89957	0.06207	0.06203	0.75722	0.7624	0.5384	0.53863	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42482	42482	SRR5639266	SRX2877666	SRS2249443	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 6	GSM2646587	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 6	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646587	GSM2646587: MYC 6; Danio rerio; RNA Seq	GSM2646587		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646587	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-6_MWZ3676_S6_R2_001.fastq.gz 20161116_MYC-6_MWZ3676_S6_R1_001.fastq.gz	fastq fastq	9715852500.0	64772350.0	GSM2646587 r1	0:75 1:75	A:2676443912;C:2226149175;G:2271136868;T:2537875397;N:4247148	75	75	2676443912	2226149175	2271136868	2537875397	4247148	SRX2877666	SRS2249443	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.90528	0.90734	0.07913	0.07931	0.76694	0.77258	0.58608	0.58389	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42483	42483	SRR5639265	SRX2877665	SRS2249440	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 5	GSM2646586	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 5	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646586	GSM2646586: MYC 5; Danio rerio; RNA Seq	GSM2646586		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646586	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-5_MWZ3676_S5_R1_001.fastq.gz 20161116_MYC-5_MWZ3676_S5_R2_001.fastq.gz	fastq fastq	9009014700.0	60060098.0	GSM2646586 r1	0:75 1:75	A:2448288707;C:2095898874;G:2134585761;T:2326368656;N:3872702	75	75	2448288707	2095898874	2134585761	2326368656	3872702	SRX2877665	SRS2249440	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.90528	0.90592	0.08568	0.08499	0.76589	0.77232	0.56872	0.57864	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42484	42484	SRR5639264	SRX2877664	SRS2249442	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 4	GSM2646585	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 4	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646585	GSM2646585: MYC 4; Danio rerio; RNA Seq	GSM2646585		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646585	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-4_MWZ3676_S4_R1_001.fastq.gz 20161116_MYC-4_MWZ3676_S4_R2_001.fastq.gz	fastq fastq	8514092237.0	60342948.0	GSM2646585 r1	0:75 1:75.00	A:2362847360;C:1933488006;G:1961930272;T:2252168244;N:3658355	75	75	2362847360	1933488006	1961930272	2252168244	3658355	SRX2877664	SRS2249442	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.91098	0.91363	0.06049	0.06082	0.75237	0.75785	0.52723	0.44724	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42485	42485	SRR5639263	SRX2877663	SRS2249439	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 3	GSM2646584	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 3	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646584	GSM2646584: MYC 3; Danio rerio; RNA Seq	GSM2646584		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646584	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-3_MWZ3676_S3_R1_001.fastq.gz 20161116_MYC-3_MWZ3676_S3_R2_001.fastq.gz	fastq fastq	9499251600.0	63328344.0	GSM2646584 r1	0:75 1:75	A:2600983566;C:2193461949;G:2224307535;T:2476379293;N:4119257	75	75	2600983566	2193461949	2224307535	2476379293	4119257	SRX2877663	SRS2249439	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.9202	0.92206	0.07816	0.07901	0.74612	0.75268	0.55199	0.54541	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42486	42486	SRR5639262	SRX2877662	SRS2249438	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 2	GSM2646583	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 2	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646583	GSM2646583: MYC 2; Danio rerio; RNA Seq	GSM2646583		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646583	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-2_MWZ3676_S2_R1_001.fastq.gz 20161116_MYC-2_MWZ3676_S2_R2_001.fastq.gz	fastq fastq	9916108050.0	66107387.0	GSM2646583 r1	0:75 1:75	A:2707842597;C:2295701488;G:2339804244;T:2568467441;N:4292280	75	75	2707842597	2295701488	2339804244	2568467441	4292280	SRX2877662	SRS2249438	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.91755	0.91847	0.06435	0.06371	0.76721	0.77277	0.57525	0.58163	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42487	42487	SRR5639261	SRX2877661	SRS2249437	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYC 1	GSM2646582	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYC 1	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYC transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646582	GSM2646582: MYC 1; Danio rerio; RNA Seq	GSM2646582		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646582	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161116_MYC-1_MWZ3676_S1_R1_001.fastq.gz 20161116_MYC-1_MWZ3676_S1_R2_001.fastq.gz	fastq fastq	9133899450.0	60892663.0	GSM2646582 r1	0:75 1:75	A:2485889577;C:2124525486;G:2159911091;T:2359614852;N:3958444	75	75	2485889577	2124525486	2159911091	2359614852	3958444	SRX2877661	SRS2249437	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.92038	0.92088	0.07532	0.07511	0.74811	0.75576	0.58853	0.58804	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42488	42488	SRR5639260	SRX2877660	SRS2249436	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYCN 4	GSM2646581	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYCN 4	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646581	GSM2646581: MYCN 4; Danio rerio; RNA Seq	GSM2646581		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646581	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161021_WT-4_MWZ3582_S4_R1_001.fastq.gz 20161021_WT-4_MWZ3582_S4_R2_001.fastq.gz	fastq fastq	9350290500.0	62335270.0	GSM2646581 r1	0:75 1:75	A:2584645248;C:2113813813;G:2141529817;T:2509027204;N:1274418	75	75	2584645248	2113813813	2141529817	2509027204	1274418	SRX2877660	SRS2249436	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.94127	0.94311	0.07924	0.07907	0.73673	0.74026	0.48176	0.46073	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42489	42489	SRR5639259	SRX2877659	SRS2249434	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYCN 3	GSM2646580	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYCN 3	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646580	GSM2646580: MYCN 3; Danio rerio; RNA Seq	GSM2646580		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646580	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161021_WT-3_MWZ3582_S3_R1_001.fastq.gz 20161021_WT-3_MWZ3582_S3_R2_001.fastq.gz	fastq fastq	8155574400.0	54370496.0	GSM2646580 r1	0:75 1:75	A:2218692747;C:1881082606;G:1915867614;T:2138862711;N:1068722	75	75	2218692747	1881082606	1915867614	2138862711	1068722	SRX2877659	SRS2249434	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.94262	0.94367	0.05391	0.05378	0.74631	0.75099	0.48101	0.4861	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42490	42490	SRR5639258	SRX2877658	SRS2249435	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYCN 2	GSM2646579	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYCN 2	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646579	GSM2646579: MYCN 2; Danio rerio; RNA Seq	GSM2646579		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646579	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161021_WT-2_MWZ3582_S2_R1_001.fastq.gz 20161021_WT-2_MWZ3582_S2_R2_001.fastq.gz	fastq fastq	11327208000.0	75514720.0	GSM2646579 r1	0:75 1:75	A:3089154339;C:2598817018;G:2660297425;T:2977379789;N:1559429	75	75	3089154339	2598817018	2660297425	2977379789	1559429	SRX2877658	SRS2249435	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.94797	0.95019	0.06855	0.06894	0.75028	0.75386	0.51196	0.50362	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
42491	42491	SRR5639257	SRX2877657	SRS2249433	SRP108529	PRJNA388953	c MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA Seq]	GSE99567	Transcriptome Analysis	Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors 11% express high levels of c MYC MYC protein. To study this newly defined subgroup we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early onset neuroblastoma. Overall design: RNA seq was performed on MYC and MYCN driven neuroblastoma tumors to determine chromatin accesibility in these cells	parent bioproject:PRJNA388873		MYCN 1	GSM2646578	tissue:EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.\|cell type:EGFP+ neuroblasts	MYCN 1	Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence using cutadapt then mapped to dr7 whole genome using Tophat 2.0.11 without xxx splicing form calls Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. FPKM values were used to normalize and quantify each transcripts Genome build: dr7 Supplementary files format and content: excel files include RPKM values for each Sample ...	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN transgenic zebrafish.		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ neuroblasts	GSM2646578	GSM2646578: MYCN 1; Danio rerio; RNA Seq	GSM2646578		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2646578	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP108529	20161021_WT-1_MWZ3582_S1_R1_001.fastq.gz 20161021_WT-1_MWZ3582_S1_R2_001.fastq.gz	fastq fastq	11581106850.0	77207379.0	GSM2646578 r1	0:75 1:75	A:3217356977;C:2602411576;G:2673363734;T:3086367856;N:1606707	75	75	3217356977	2602411576	2673363734	3086367856	1606707	SRX2877657	SRS2249433	SRA569347	GEO	Oncology/Hematology, Boston Children's Hospital	2	0.94008	0.94168	0.08272	0.08234	0.72784	0.73283	0.50397	0.49362	75	75	B	B	biological fallback assumption	illumina	hiseq_era	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-06-01	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44955	44955	SRR6334491	SRX3433619	SRS2724937	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	MYCNoe r4	GSM2870458	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	MYCNoe r4	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	GSM2870458	GSM2870458: MYCNoe r4; Danio rerio; RNA Seq	GSM2870458		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870458	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	MYCNoe_r4.20161021_WT-4_MWZ3582_S4_R1_001.fastq.gz MYCNoe_r4.20161021_WT-4_MWZ3582_S4_R2_001.fastq.gz	fastq fastq	9350290500.0	62335270.0	GSM2870458 r1	0:75 1:75	A:2584645248;C:2113813813;G:2141529817;T:2509027204;N:1274418	75	75	2584645248	2113813813	2141529817	2509027204	1274418	SRX3433619	SRS2724937	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94125	0.94312	0.07937	0.07925	0.73667	0.7405	0.48297	0.46234	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44956	44956	SRR6334490	SRX3433618	SRS2724936	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	MYCNoe r3	GSM2870457	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	MYCNoe r3	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	GSM2870457	GSM2870457: MYCNoe r3; Danio rerio; RNA Seq	GSM2870457		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870457	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	MYCNoe_r3.20161021_WT-3_MWZ3582_S3_R2_001.fastq.gz MYCNoe_r3.20161021_WT-3_MWZ3582_S3_R1_001.fastq.gz	fastq fastq	8155574400.0	54370496.0	GSM2870457 r1	0:75 1:75	A:2218692747;C:1881082606;G:1915867614;T:2138862711;N:1068722	75	75	2218692747	1881082606	1915867614	2138862711	1068722	SRX3433618	SRS2724936	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94262	0.94367	0.05384	0.05359	0.74629	0.75097	0.48167	0.48775	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44957	44957	SRR6334489	SRX3433617	SRS2724935	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	MYCNoe r2	GSM2870456	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	MYCNoe r2	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	GSM2870456	GSM2870456: MYCNoe r2; Danio rerio; RNA Seq	GSM2870456		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870456	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	MYCNoe_r2.20161021_WT-2_MWZ3582_S2_R2_001.fastq.gz MYCNoe_r2.20161021_WT-2_MWZ3582_S2_R1_001.fastq.gz	fastq fastq	11327208000.0	75514720.0	GSM2870456 r1	0:75 1:75	A:3089154339;C:2598817018;G:2660297425;T:2977379789;N:1559429	75	75	3089154339	2598817018	2660297425	2977379789	1559429	SRX3433617	SRS2724935	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94799	0.95014	0.06824	0.06879	0.75012	0.75396	0.5118	0.50287	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44958	44958	SRR6334488	SRX3433616	SRS2724934	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	MYCNoe r1	GSM2870455	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	MYCNoe r1	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:n Myc	GSM2870455	GSM2870455: MYCNoe r1; Danio rerio; RNA Seq	GSM2870455		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870455	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	MYCNoe_r1.20161021_WT-1_MWZ3582_S1_R2_001.fastq.gz MYCNoe_r1.20161021_WT-1_MWZ3582_S1_R1_001.fastq.gz	fastq fastq	11581106850.0	77207379.0	GSM2870455 r1	0:75 1:75	A:3217356977;C:2602411576;G:2673363734;T:3086367856;N:1606707	75	75	3217356977	2602411576	2673363734	3086367856	1606707	SRX3433616	SRS2724934	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94008	0.94163	0.08278	0.08227	0.7276	0.73255	0.50145	0.49414	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44959	44959	SRR6334487	SRX3433615	SRS2724933	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line2 r4	GSM2870454	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line2 r4	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870454	GSM2870454: cMYCoe line2 r4; Danio rerio; RNA Seq	GSM2870454		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870454	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line2_r4.20161116_MYC-8_MWZ3676_S8_R2_001.fastq.gz cMYCoe_line2_r4.20161116_MYC-8_MWZ3676_S8_R1_001.fastq.gz	fastq fastq	10081869900.0	67212466.0	GSM2870454 r1	0:75 1:75	A:2790689900;C:2299822096;G:2324357632;T:2662657984;N:4342288	75	75	2790689900	2299822096	2324357632	2662657984	4342288	SRX3433615	SRS2724933	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.90219	0.90342	0.05116	0.05047	0.75091	0.75554	0.53057	0.44417	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44960	44960	SRR6334486	SRX3433614	SRS2724932	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line2 r3	GSM2870453	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line2 r3	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870453	GSM2870453: cMYCoe line2 r3; Danio rerio; RNA Seq	GSM2870453		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870453	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line2_r3.20161116_MYC-7_MWZ3676_S7_R1_001.fastq.gz cMYCoe_line2_r3.20161116_MYC-7_MWZ3676_S7_R2_001.fastq.gz	fastq fastq	9707643300.0	64717622.0	GSM2870453 r1	0:75 1:75	A:2656490466;C:2245711917;G:2271269818;T:2529962783;N:4208316	75	75	2656490466	2245711917	2271269818	2529962783	4208316	SRX3433614	SRS2724932	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.89705	0.89958	0.06199	0.06253	0.75706	0.76232	0.54548	0.53954	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44961	44961	SRR6334485	SRX3433613	SRS2724931	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line2 r2	GSM2870452	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line2 r2	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870452	GSM2870452: cMYCoe line2 r2; Danio rerio; RNA Seq	GSM2870452		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870452	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line2_r2.20161116_MYC-6_MWZ3676_S6_R1_001.fastq.gz cMYCoe_line2_r2.20161116_MYC-6_MWZ3676_S6_R2_001.fastq.gz	fastq fastq	9715852500.0	64772350.0	GSM2870452 r1	0:75 1:75	A:2676443912;C:2226149175;G:2271136868;T:2537875397;N:4247148	75	75	2676443912	2226149175	2271136868	2537875397	4247148	SRX3433613	SRS2724931	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.90529	0.90731	0.07869	0.0794	0.7669	0.77242	0.59274	0.5848	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44962	44962	SRR6334484	SRX3433612	SRS2724930	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line2 r1	GSM2870451	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line2 r1	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870451	GSM2870451: cMYCoe line2 r1; Danio rerio; RNA Seq	GSM2870451		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870451	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line2_r1.20161116_MYC-5_MWZ3676_S5_R2_001.fastq.gz cMYCoe_line2_r1.20161116_MYC-5_MWZ3676_S5_R1_001.fastq.gz	fastq fastq	9009014700.0	60060098.0	GSM2870451 r1	0:75 1:75	A:2448288707;C:2095898874;G:2134585761;T:2326368656;N:3872702	75	75	2448288707	2095898874	2134585761	2326368656	3872702	SRX3433612	SRS2724930	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.90529	0.9059	0.08558	0.08533	0.76654	0.77252	0.56588	0.57792	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44963	44963	SRR6334483	SRX3433611	SRS2724929	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line1 r4	GSM2870450	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line1 r4	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870450	GSM2870450: cMYCoe line1 r4; Danio rerio; RNA Seq	GSM2870450		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870450	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line1_r4.20161116_MYC-4_MWZ3676_S4_R2_001.fastq.gz cMYCoe_line1_r4.20161116_MYC-4_MWZ3676_S4_R1_001.fastq.gz	fastq fastq	9051442200.0	60342948.0	GSM2870450 r1	0:75 1:75	A:2512441086;C:2054230579;G:2086517596;T:2394346120;N:3906819	75	75	2512441086	2054230579	2086517596	2394346120	3906819	SRX3433611	SRS2724929	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.91137	0.91373	0.06085	0.06087	0.74424	0.75035	0.43441	0.53176	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44964	44964	SRR6334482	SRX3433610	SRS2724928	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line1 r3	GSM2870449	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line1 r3	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870449	GSM2870449: cMYCoe line1 r3; Danio rerio; RNA Seq	GSM2870449		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870449	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line1_r3.20161116_MYC-3_MWZ3676_S3_R1_001.fastq.gz cMYCoe_line1_r3.20161116_MYC-3_MWZ3676_S3_R2_001.fastq.gz	fastq fastq	9499251600.0	63328344.0	GSM2870449 r1	0:75 1:75	A:2600983566;C:2193461949;G:2224307535;T:2476379293;N:4119257	75	75	2600983566	2193461949	2224307535	2476379293	4119257	SRX3433610	SRS2724928	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.92026	0.92207	0.0781	0.07917	0.74663	0.75284	0.55184	0.54485	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44965	44965	SRR6334481	SRX3433609	SRS2724927	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line1 r2	GSM2870448	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line1 r2	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870448	GSM2870448: cMYCoe line1 r2; Danio rerio; RNA Seq	GSM2870448		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870448	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line1_r2.20161116_MYC-2_MWZ3676_S2_R1_001.fastq.gz cMYCoe_line1_r2.20161116_MYC-2_MWZ3676_S2_R2_001.fastq.gz	fastq fastq	9916108050.0	66107387.0	GSM2870448 r1	0:75 1:75	A:2707842597;C:2295701488;G:2339804244;T:2568467441;N:4292280	75	75	2707842597	2295701488	2339804244	2568467441	4292280	SRX3433609	SRS2724927	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.91753	0.91846	0.06388	0.06359	0.76702	0.77258	0.57242	0.58362	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
44966	44966	SRR6334480	SRX3433608	SRS2724926	SRP125946	PRJNA420576	c MYC drives a subset of high risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA seq]	GSE107518	Transcriptome Analysis	Childhood neuroblastoma is known for MYCN gene amplification and here we show that in a separate subset of cases MYC itself is activated due to enhancer hijacking from chromosomal translocations or duplications thus defining a unique subset of high risk disease. Overall design: RNA seq in zebrafish overexpressing human c Myc or n Myc	parent bioproject:PRJNA398387	pubmed:29284669	cMYCoe line1 r1	GSM2870447	tissue:Neuroblastoma tumor cells\|cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	cMYCoe line1 r1	Reads were aligned to a custom version of the zebrafish reference genome containing danRer10 references for all zebrafish chromosomes and "pseudochromosomes" created from the coding sequence of human c Myc and n Myc used in the experimental system Reads were aligned using tophat with parameters no novel juncs and in single end mode Read counts per RefSeq gene and human c Myc and n Myc were quantified using htseq count using parameters stranded=no i gene name f bam Reads per kilobase of exon per million mapped reads were created from these readcounts by dividing by the number of kilobases in all isoforms with the same gene name and then by the millions of mapped reads Supplementary files format and content: WIG filess represent counts of aligned reads within 50 bp bins with each read being extended 200 in the direction of alignment. Counts are in reads per million and floored at 0.1	Neuroblastoma tumor cells		Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	EGFP+ neuroblastoma cells were harvested from tumor bearing MYCN and MYC transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ cells were sorted directly into Trizol LS	cell type:EGFP+ transformed neuroblasts\|overexpression:c Myc	GSM2870447	GSM2870447: cMYCoe line1 r1; Danio rerio; RNA Seq	GSM2870447		1	Sorted EGFP+ cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on a HiSeq Illumina sequencer with 2x100bp paired end reads.	GEO Accession:GSM2870447	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP125946	cMYCoe_line1_r1.20161116_MYC-1_MWZ3676_S1_R2_001.fastq.gz cMYCoe_line1_r1.20161116_MYC-1_MWZ3676_S1_R1_001.fastq.gz	fastq fastq	9133899450.0	60892663.0	GSM2870447 r1	0:75 1:75	A:2485889577;C:2124525486;G:2159911091;T:2359614852;N:3958444	75	75	2485889577	2124525486	2159911091	2359614852	3958444	SRX3433608	SRS2724926	SRA634977	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.92038	0.92085	0.07527	0.07547	0.74848	0.75562	0.58873	0.58813	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2017-11-29	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
46223	46223	SRR6507310	SRX3595752	SRS2864724	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	MPNST 3	GSM2946791	tissue:malignant peripheral nerve sheath tumor\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	MPNST 3	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	malignant peripheral nerve sheath tumor	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	GSM2946791	GSM2946791: MPNST 3; Danio rerio; RNA Seq	GSM2946791		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946791	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	MPNST_3.bam	bam	11383285396.0	56352898.0	GSM2946791 r1	0:101 1:101	A:3079386367;C:2613075331;G:2617162315;T:3072644029;N:1017354	101	101	3079386367	2613075331	2617162315	3072644029	1017354	SRX3595752	SRS2864724	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.92421	0.92754	0.11361	0.112	0.69203	0.69365	0.47226	0.47658	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46224	46224	SRR6507309	SRX3595751	SRS2864311	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	MPNST 2	GSM2946790	tissue:malignant peripheral nerve sheath tumor\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	MPNST 2	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	malignant peripheral nerve sheath tumor	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	GSM2946790	GSM2946790: MPNST 2; Danio rerio; RNA Seq	GSM2946790		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946790	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	MPNST_2.bam	bam	4475755208.0	22157204.0	GSM2946790 r1	0:101 1:101	A:1173881184;C:1063354569;G:1068337599;T:1169755139;N:426717	101	101	1173881184	1063354569	1068337599	1169755139	426717	SRX3595751	SRS2864311	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.94771	0.95125	0.06684	0.06559	0.72427	0.72634	0.48094	0.48917	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46225	46225	SRR6507308	SRX3595750	SRS2864123	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	MPNST 1	GSM2946789	tissue:malignant peripheral nerve sheath tumor\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	MPNST 1	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	malignant peripheral nerve sheath tumor	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant dissection	GSM2946789	GSM2946789: MPNST 1; Danio rerio; RNA Seq	GSM2946789		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946789	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	MPNST_1.bam	bam	4758494608.0	23556904.0	GSM2946789 r1	0:101 1:101	A:1256101624;C:1121363306;G:1131796356;T:1248769939;N:463383	101	101	1256101624	1121363306	1131796356	1248769939	463383	SRX3595750	SRS2864123	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.94674	0.9501	0.07974	0.07759	0.70761	0.71155	0.48864	0.49029	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46226	46226	SRR6507307	SRX3595749	SRS2864137	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	Leukemia 3	GSM2946788	tissue:Natural Killer cell leukemia\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	Leukemia 3	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	Natural Killer cell leukemia	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	GSM2946788	GSM2946788: Leukemia 3; Danio rerio; RNA Seq	GSM2946788		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946788	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	Leukemia_3.bam	bam	4769595114.0	23611857.0	GSM2946788 r1	0:101 1:101	A:1234057643;C:1141479035;G:1156554815;T:1237033403;N:470218	101	101	1234057643	1141479035	1156554815	1237033403	470218	SRX3595749	SRS2864137	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.94945	0.95271	0.09019	0.0888	0.74777	0.74963	0.47913	0.47856	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46227	46227	SRR6507306	SRX3595748	SRS2864295	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	Leukemia 2	GSM2946787	tissue:Natural Killer cell leukemia\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	Leukemia 2	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	Natural Killer cell leukemia	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	GSM2946787	GSM2946787: Leukemia 2; Danio rerio; RNA Seq	GSM2946787		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946787	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	Leukemia_2.bam	bam	3932585692.0	19468246.0	GSM2946787 r1	0:101 1:101	A:1026642167;C:937784785;G:940180391;T:1027590540;N:387809	101	101	1026642167	937784785	940180391	1027590540	387809	SRX3595748	SRS2864295	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.93844	0.93922	0.13853	0.13474	0.75765	0.76023	0.48216	0.49502	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46228	46228	SRR6507305	SRX3595747	SRS2864135	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	Leukemia 1	GSM2946786	tissue:Natural Killer cell leukemia\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	Leukemia 1	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	Natural Killer cell leukemia	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	GSM2946786	GSM2946786: Leukemia 1; Danio rerio; RNA Seq	GSM2946786		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946786	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	Leukemia_1.bam	bam	5514990264.0	27301932.0	GSM2946786 r1	0:101 1:101	A:1473054210;C:1283289156;G:1289375636;T:1468738366;N:532896	101	101	1473054210	1283289156	1289375636	1468738366	532896	SRX3595747	SRS2864135	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.93575	0.93936	0.12916	0.12725	0.74097	0.74312	0.47845	0.48929	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46229	46229	SRR6507304	SRX3595746	SRS2864134	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	Angiosarcoma 2	GSM2946785	tissue:angiosarcoma\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	Angiosarcoma 2	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	angiosarcoma	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	GSM2946785	GSM2946785: Angiosarcoma 2; Danio rerio; RNA Seq	GSM2946785		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946785	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	Angiosarcoma_2.bam	bam	5653646094.0	27988347.0	GSM2946785 r1	0:101 1:101	A:1527009041;C:1301975169;G:1301292898;T:1522816041;N:552945	101	101	1527009041	1301975169	1301292898	1522816041	552945	SRX3595746	SRS2864134	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.93396	0.93929	0.10315	0.1009	0.67065	0.67322	0.4792	0.47967	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
46230	46230	SRR6507303	SRX3595745	SRS2864133	SRP131267	PRJNA431425	tp53 deficiency causes a wide tumor spectrum and elevates embryonal rhabdomyosarcoma metastasis in zebrafish	GSE109581	Transcriptome Analysis	We generated tp53 deletion mutant zebrafish that spontaneously develop malignant peripheral nerve sheath tumors angiosarcomas germ cell tumors and an aggressive Natural Killer cell leukemia not previously reported in zebrafish. Each tumor type efficiently engrafted into syngeneic recipient zebrafish and shared gene expression signatures with predicted cells of origin. Overall design: We generated a complete null tp53 deletion allele in syngeneic CG1 strain zebrafish using TALEN endonucleases. The list of tumors spontaneously developed in these tp53del/del animals included malignant peripheral nerve sheath tumors MPNSTs angiosarcomas germ cell tumors and Natural Killer cell leukemia. We obtained 3 MPNSTs samples MPNST 1 MPNST 2 and MPNST 3 2 angiosarcoma samples Angiosarcoma 1 and Angiosarcoma 2 3 leukemia samples Leukemia 1 Leukemia 2 and Leukemia 3 and 1 sample of germ cell tumor GermCell 1. We also assessed the role of tp53 in kRASG12D induced human embryonal rhabdomyosarcoma ERMS using large scale cell transplantation assays and live fluorescent imaging over time. We obtained 3 ERMS samples ERMS 1 ERMS 2 and ERMS 3. All these tumor samples were compared to 3 background CG1 samples samples WholeFish 1 WholeFish 2 and WholeFish 3.		pubmed:30192230	Angiosarcoma 1	GSM2946784	tissue:angiosarcoma\|genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	Angiosarcoma 1	Reads were aligned with STAR v2.4.0; PCR duplicates were removed with Picard v1.95 and reads aligning to ribosomal RNA were removed with RSeQC; gene counts were obtained from reads with an alignment quality of at least 10 using featureCounts and transformed to transcript per million TPM units. Genome build: GRCz10 Supplementary files format and content: Counts matrix provided as supplementary file.	angiosarcoma	Tissue was harvested using 90% PBS + 5% FBS. FACS sorting was performed to obtain tumor cell fraction with 85% purity and 90% viability.	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	Animals were raised at 28 degrees celcius	genotype:CG1 tp53 homozygous mutant\|tumor type:spontaneous\|procedure:primary transplant GFP FACS sorted	GSM2946784	GSM2946784: Angiosarcoma 1; Danio rerio; RNA Seq	GSM2946784		1	Total RNA was extracted using RLT buffer Qiagen and purified using RNeasy kit Qiagen as per manufacturer instructions Libraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit	GEO Accession:GSM2946784	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2500	SRP131267	Angiosarcoma_1.bam	bam	5694971052.0	28192926.0	GSM2946784 r1										SRX3595745	SRS2864133	SRA652013	GEO	Pathology, Massachusetts General Hospital	2	0.95498	0.93958	0.06596	0.06254	0.68594	0.68647	0.47578	0.47052	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2018-01-24	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51023	51023	SRR12429756	SRX8925578	SRS7181813	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST suz12 mut Z5	GSM4720870	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b:+/	MPNST suz12 mut Z5	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b:+/	GSM4720870	GSM4720870: MPNST suz12 mut Z5; Danio rerio; RNA Seq	GSM4720870		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM4720870	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_Z5_MWZ4474_S7_R1_001.fastq.gz 20170730_Z5_MWZ4474_S7_R2_001.fastq.gz	fastq fastq	7968086400.0	53120576.0	GSM4720870 r1	0:75 1:75	A:2175597026;C:1816735807;G:1842562950;T:2131670896;N:1519721	75	75	2175597026	1816735807	1842562950	2131670896	1519721	SRX8925578	SRS7181813	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.92871	0.92975	0.08295	0.08243	0.78263	0.79868	0.52067	0.52262	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-08-11	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51024	51024	SRR12429755	SRX8925577	SRS7181811	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST suz12 mut Z3	GSM4720869	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b:+/	MPNST suz12 mut Z3	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b:+/	GSM4720869	GSM4720869: MPNST suz12 mut Z3; Danio rerio; RNA Seq	GSM4720869		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM4720869	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_Z3_MWZ4474_S6_R1_001.fastq.gz 20170730_Z3_MWZ4474_S6_R2_001.fastq.gz	fastq fastq	7640907450.0	50939383.0	GSM4720869 r1	0:75 1:75	A:2079034539;C:1748735317;G:1754586436;T:2057075691;N:1475467	75	75	2079034539	1748735317	1754586436	2057075691	1475467	SRX8925577	SRS7181811	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.93466	0.93441	0.0777	0.07678	0.7766	0.79368	0.53878	0.53762	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-08-11	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51025	51025	SRR12429754	SRX8925576	SRS7181810	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST suz12 mut Z2	GSM4720868	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b: /	MPNST suz12 mut Z2	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b: /	GSM4720868	GSM4720868: MPNST suz12 mut Z2; Danio rerio; RNA Seq	GSM4720868		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM4720868	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_Z2_MWZ4474_S5_R1_001.fastq.gz 20170730_Z2_MWZ4474_S5_R2_001.fastq.gz	fastq fastq	7725082350.0	51500549.0	GSM4720868 r1	0:75 1:75	A:2140078104;C:1732679948;G:1742195011;T:2108639649;N:1489638	75	75	2140078104	1732679948	1742195011	2108639649	1489638	SRX8925576	SRS7181810	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.92806	0.92776	0.08381	0.0825	0.76019	0.77699	0.51452	0.53018	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-08-11	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51026	51026	SRR12429753	SRX8925575	SRS7181809	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST suz12 mut Z1	GSM4720867	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b: /	MPNST suz12 mut Z1	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt\|suz12a:+/ \|suz12b: /	GSM4720867	GSM4720867: MPNST suz12 mut Z1; Danio rerio; RNA Seq	GSM4720867		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM4720867	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_Z1_MWZ4474_S4_R2_001.fastq.gz 20170730_Z1_MWZ4474_S4_R1_001.fastq.gz	fastq fastq	5642950050.0	37619667.0	GSM4720867 r1	0:75 1:75	A:1537175203;C:1290621752;G:1298132389;T:1515946875;N:1073831	75	75	1537175203	1290621752	1298132389	1515946875	1073831	SRX8925575	SRS7181809	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.92722	0.92948	0.08526	0.08492	0.74771	0.76656	0.50026	0.51083	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-08-11	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51027	51027	SRR8439649	SRX5247079	SRS4273268	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx mut A16	GSM3561588	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	MPNST atrx mut A16	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	GSM3561588	GSM3561588: MPNST atrx mut A16; Danio rerio; RNA Seq	GSM3561588		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561588	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A16_MWZ4474_S10_R1_001.fastq.gz 20170730_A16_MWZ4474_S10_R2_001.fastq.gz	fastq fastq	8340354300.0	55602362.0	GSM3561588 r1	0:75 1:75	A:2263688783;C:1911816082;G:1926080483;T:2237169236;N:1599716	75	75	2263688783	1911816082	1926080483	2237169236	1599716	SRX5247079	SRS4273268	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.92645	0.92604	0.08416	0.08296	0.75607	0.7753	0.5085	0.5092	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51028	51028	SRR8439648	SRX5247078	SRS4273267	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx mut A15	GSM3561587	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	MPNST atrx mut A15	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	GSM3561587	GSM3561587: MPNST atrx mut A15; Danio rerio; RNA Seq	GSM3561587		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561587	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A15_MWZ4474_S9_R1_001.fastq.gz 20170730_A15_MWZ4474_S9_R2_001.fastq.gz	fastq fastq	8241576300.0	54943842.0	GSM3561587 r1	0:75 1:75	A:2288402334;C:1835846255;G:1874705276;T:2241015118;N:1607317	75	75	2288402334	1835846255	1874705276	2241015118	1607317	SRX5247078	SRS4273267	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.93509	0.93468	0.08306	0.08245	0.77506	0.79458	0.56347	0.58112	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51029	51029	SRR8439647	SRX5247077	SRS4273266	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx mut A1	GSM3561586	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	MPNST atrx mut A1	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:+/	GSM3561586	GSM3561586: MPNST atrx mut A1; Danio rerio; RNA Seq	GSM3561586		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561586	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A1_MWZ4474_S3_R2_001.fastq.gz 20170730_A1_MWZ4474_S3_R1_001.fastq.gz	fastq fastq	7091090550.0	47273937.0	GSM3561586 r1	0:75 1:75	A:1979016948;C:1575512434;G:1582806544;T:1952381152;N:1373472	75	75	1979016948	1575512434	1582806544	1952381152	1373472	SRX5247077	SRS4273266	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.91956	0.91956	0.08912	0.0878	0.74848	0.76627	0.52338	0.51896	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51030	51030	SRR8439646	SRX5247076	SRS4273265	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx WT A14	GSM3561585	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	MPNST atrx WT A14	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	GSM3561585	GSM3561585: MPNST atrx WT A14; Danio rerio; RNA Seq	GSM3561585		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561585	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A14_MWZ4474_S8_R1_001.fastq.gz 20170730_A14_MWZ4474_S8_R2_001.fastq.gz	fastq fastq	6664823700.0	44432158.0	GSM3561585 r1	0:75 1:75	A:1818800880;C:1519582626;G:1528375916;T:1796781856;N:1282422	75	75	1818800880	1519582626	1528375916	1796781856	1282422	SRX5247076	SRS4273265	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.92705	0.92717	0.08967	0.0892	0.75209	0.7709	0.50996	0.49376	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51031	51031	SRR8439645	SRX5247075	SRS4273263	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx WT A11	GSM3561584	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	MPNST atrx WT A11	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	GSM3561584	GSM3561584: MPNST atrx WT A11; Danio rerio; RNA Seq	GSM3561584		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561584	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A11_MWZ4474_S2_R1_001.fastq.gz 20170730_A11_MWZ4474_S2_R2_001.fastq.gz	fastq fastq	6371036850.0	42473579.0	GSM3561584 r1	0:75 1:75	A:1739144818;C:1449791284;G:1464375008;T:1716495405;N:1230335	75	75	1739144818	1449791284	1464375008	1716495405	1230335	SRX5247075	SRS4273263	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.9254	0.92615	0.08446	0.08397	0.74945	0.76761	0.51446	0.51395	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
51032	51032	SRR8439644	SRX5247074	SRS4273264	SRP180876	PRJNA515051	Zebrafish Samples for Loss of ATRX cooperates with p53 Deficiency to promote the Development of Sarcomas and other Malignancies	GSE125040	Transcriptome Analysis	The SWI/SNF family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres ALT pathway in tumor cells while it also affects Polycomb repressive complex 2 PRC2 silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis we knocked out atrx in our previously published p53/nf1 deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR cas9 was lethal in developing fish and resulted in an alpha thalassemia like phenotype including reduced alpha globin expression. In p53/nf1 deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/ fish but these fish developed various tumors that were not observed in their atrx+/+ siblings including epithelioid sarcoma angiosarcoma undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX indicating that our zebrafish model reliably reflects a role for ATRX loss in the early pathogenesis of these types of human cancers. RNA seq of p53/nf1 and p53/nf1/atrx deficient tumors revealed that down regulation of telomerase accompanied ALT mediated lengthening of the telomeres in atrx mutant samples. Moreover inactivating mutations in atrx disturbed PRC2 target gene silencing indicating a connection between ATRX loss and PRC2 dysfunction in cancer development. Overall design: Gene expression values were derived from paired end RNA Seq data that compared zebrafish samples from p53/nf1/atrx deficient tumors to samples from atrx wildtype controls 3 vs. 3 samples.		pubmed:30970016;pubmed:32651197	MPNST atrx WT A9	GSM3561583	tissue:Zebrafish malignant peripheral nerve sheath tumors MPNSTs\|tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	MPNST atrx WT A9	FastQC was used to evaluate read quality on raw RNA Seq reads and trimmed reads. Trimming of low quality reads and clipping of sequencing adapters was done using the program Trimmomatic version 0.36 and all reads shorter than 36bp post trimming were dropped Trimmomatic was run with settings of ILLUMINACLIP:adapters/TruSeq3 PE 2.fa: 2:30:10 LEADING:3 TRAILING:3 SLIDINGWINDOW:4:15 MINLEN:36 AVGQUAL:10. Reads were aligned to the zebrafish Danio rerio reference genome with TopHat version 2.1.0 using UCSC danRer10 and settings of x 1 g 1 r 44 mate std dev 223 with values for the flags r and mate std dev coming from the mean fragment size. Bam sorting and indexing was done with SamTools and duplicate reads were removed using Picard tools http://picard.sourceforge.net. Aligned reads processed to Fragments Per Kilobase of exon per Million fragments mapped FPKM using cufflinks version 2.2.1 http://cufflinks.cbcb.umd.edu/index.html with the G flag to use the danRer10 reference annotation to estimate isoform expression and not assemble novel transcripts and the flags max bundle frags 4000000 N compatible hits norm. Gene level counts were obtained with htseq count version 0.9.1. Differential gene expression was evaluated with the R Bioconductor package DESeq2 and normalized expression values for individual samples were obtained from DESeq2 using the variance stabilizing transform on the raw counts. The variance stabilizing transformed data were used for GSEA. Genome build: GRCz10 Supplementary files format and content: genes.fpkm tracking files are tab delimited text files output by cufflinks in a generic FPKM tracking format with estimated gene level expression values in the form of FPKM values and raw count.txt files are tab delimited text files output by htseq count with gene level counts	Zebrafish malignant peripheral nerve sheath tumors MPNSTs	The zebrafish atrx mutant lines were generated by the CRISPR Cas9 genome editing system using the previous described protocol Hwang et al. Nature Biotechnology 2013. The plasmid constructs pDR274 #42250 and pMLM3613 #42251 were purchased from Addgene. Oligonucleotides 5’ TAG GTC CTG AGT TCC GTA ACA A 3’ and 5’ AAA CTT GTT ACG GAA CTC AGG A 3’ were annealed and cloned into the pDR274 vector to generate single guide RNAs gRNAs targeting atrx exon 4. Each embryo was injected with 1 nl of solution containing 25 ng/μl gRNA and 600 ng/μl Cas9 mRNA at the 1 cell stage. Mosaic F0 fish with germline mutation were identified and stable mutant lines were established by outcrossing.	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	Zebrafish were raised and maintained according to standard procedures. They were derived from the p53/nf1 deficient background Shin et al. Disease Models & Mechanisms 2012. All zebrafish studies and maintenance were done in accord with Dana Farber Cancer Institute IACUC approved protocol #02 107.	tp53: / \|nf1b: / \|nf1a:+/ \|atrx:wt	GSM3561583	GSM3561583: MPNST atrx WT A9; Danio rerio; RNA Seq	GSM3561583		1	RNA was isolated from one half of p53/nf1/atrx deficient MPNSTs and p53/nf1 deficient control MPNSTs using the AllPrep DNA/RNA Mini Kit from Qiagen Hilden Germany and the other half was set asside for analysis by histopathology. Library preparation quality control and next generation sequencing were conducted by the Molecular Biology Core Facility of the Dana Farber Cancer Institute following standard protocols.	GEO Accession:GSM3561583	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP180876	20170730_A9_MWZ4474_S1_R1_001.fastq.gz 20170730_A9_MWZ4474_S1_R2_001.fastq.gz	fastq fastq	5832640200.0	38884268.0	GSM3561583 r1	0:75 1:75	A:1615650762;C:1304790543;G:1316843551;T:1594225635;N:1129709	75	75	1615650762	1304790543	1316843551	1594225635	1129709	SRX5247074	SRS4273264	SRA834478	GEO	Pediatric Oncology, Dana-Farber Cancer Institute	2	0.9265	0.92606	0.09204	0.09207	0.76305	0.78084	0.49678	0.50423	75	75	B	B	biological fallback assumption	illumina	nextseq	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2019-01-14	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52257	52257	SRR9067641	SRX5843745	SRS4768677	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN only 3	GSM3768994	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	MYCN only 3	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	GSM3768994	GSM3768994: MYCN only 3; Danio rerio; RNA Seq	GSM3768994		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768994	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_only_3_R1.fastq.gz MYCN_only_3_R2.fastq.gz	fastq fastq	8238967940.0	40786970.0	GSM3768994 r1	0:101 1:101	A:1930975362;C:2171935296;G:2189310816;T:1942248951;N:4497515	101	101	1930975362	2171935296	2189310816	1942248951	4497515	SRX5843745	SRS4768677	SRA887417	GEO	Mayo Clinic	2	0.83502	0.83598	0.31797	0.31379	0.73223	0.73227	0.53008	0.50101	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52258	52258	SRR9067640	SRX5843744	SRS4768676	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN only 2	GSM3768993	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	MYCN only 2	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	GSM3768993	GSM3768993: MYCN only 2; Danio rerio; RNA Seq	GSM3768993		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768993	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_only_2_R1.fastq.gz MYCN_only_2_R2.fastq.gz	fastq fastq	6418877442.0	31776621.0	GSM3768993 r1	0:101 1:101	A:1465101544;C:1733018049;G:1752009113;T:1465235986;N:3512750	101	101	1465101544	1733018049	1752009113	1465235986	3512750	SRX5843744	SRS4768676	SRA887417	GEO	Mayo Clinic	2	0.77	0.78959	0.29287	0.29725	0.73955	0.73772	0.51337	0.53486	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52259	52259	SRR9067639	SRX5843743	SRS4768675	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN only 1	GSM3768992	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	MYCN only 1	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression only	GSM3768992	GSM3768992: MYCN only 1; Danio rerio; RNA Seq	GSM3768992		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768992	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_only_1_R1.fastq.gz MYCN_only_1_R2.fastq.gz	fastq fastq	7805035378.0	38638789.0	GSM3768992 r1	0:101 1:101	A:1937052027;C:1952150867;G:1975095434;T:1936472131;N:4264919	101	101	1937052027	1952150867	1975095434	1936472131	4264919	SRX5843743	SRS4768675	SRA887417	GEO	Mayo Clinic	2	0.83391	0.83675	0.33943	0.33988	0.72058	0.72214	0.54093	0.53711	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52260	52260	SRR9067638	SRX5843742	SRS4768674	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN gas7mut 3	GSM3768991	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	MYCN gas7mut 3	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	GSM3768991	GSM3768991: MYCN gas7mut 3; Danio rerio; RNA Seq	GSM3768991		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768991	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_gas7mut_3_R1.fastq.gz MYCN_gas7mut_3_R2.fastq.gz	fastq fastq	13745995768.0	68049484.0	GSM3768991 r1	0:101 1:101	A:3255019440;C:3578390620;G:3610888877;T:3294405536;N:7291295	101	101	3255019440	3578390620	3610888877	3294405536	7291295	SRX5843742	SRS4768674	SRA887417	GEO	Mayo Clinic	2	0.89177	0.89258	0.31285	0.30575	0.72178	0.72287	0.50962	0.44338	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52261	52261	SRR9067637	SRX5843741	SRS4768673	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN gas7mut 2	GSM3768990	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	MYCN gas7mut 2	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	GSM3768990	GSM3768990: MYCN gas7mut 2; Danio rerio; RNA Seq	GSM3768990		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768990	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_gas7mut_2_R1.fastq.gz MYCN_gas7mut_2_R2.fastq.gz	fastq fastq	13284959048.0	65767124.0	GSM3768990 r1	0:101 1:101	A:2963628327;C:3652078170;G:3688732159;T:2973533051;N:6987341	101	101	2963628327	3652078170	3688732159	2973533051	6987341	SRX5843741	SRS4768673	SRA887417	GEO	Mayo Clinic	2	0.87991	0.88054	0.30981	0.31774	0.73308	0.73434	0.58824	0.5711	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52262	52262	SRR9067636	SRX5843740	SRS4768672	SRP198600	PRJNA543225	GAS7 Deficiency Promotes Metastasis of MYCN driven Neuroblastoma	GSE131307	Transcriptome Analysis	Neuroblastoma NB the most common extracranial solid tumor in children often metastasizes at a high rate. Here we demonstrate that loss of function of the growth arrest specific 7 gene GAS7 located on Chr17p13.1 a deleted region in a subset of high risk NB accelerates dissemination of MYCN overexpressing tumor cells in both zebrafish and xenografted mice models. Transcriptomic analysis of neuroblasotma tumors isolated from transgenic zebrafish overexpressing MYCN oncogene alone or MYCN with knockout of gas7 gene revealed that gene signitures affecting tumor cell cell or cell extracellular matrix interactions are significantly downregulated in tumors with gas7 loss of function. Our results provide the first genetic evidence that loss of function of a gene located in the Chr17p region contributes significantly to NB metastasis. Overall design: Examination of the transcriptomic profiles of neuroblastomas arose from transgenic fish overexpressing MYCN alone or MYCN with knockout of gas7.		pubmed:33602789	MYCN gas7mut 1	GSM3768989	source name:zebrafish tumor\|tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	MYCN gas7mut 1	Fastq files of pair end RNA Seq reads were aligned with Tophat 2.0.14 to the reference genome UCSC danRer10 using Bowtie2 2.2.6 with default parameters. Gene level counts were obtained using featureCounts 1.4.6 from the subRead package with gene models from corresponding UCSC annotation packages. Genome build: danRer10 Supplementary files format and content: tab delimited gene counts	zebrafish tumor		RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer’s instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.		tissue:peripheral sympathetic nervous system\|genotype:MYCN overexpression + gas7 knockout	GSM3768989	GSM3768989: MYCN gas7mut 1; Danio rerio; RNA Seq	GSM3768989		1	RNA was extracted from zebrafish tumors overexpressing MYCN alone or MYCN with knokcout of gas7. Total RNA was extracted using the Trizol reagent as per manufacturer's instructions. RNA integrity RIN was verified on an Agilent 2100 bioanalyzer Agilent Technologies Santa Clara CA USA and 100 200 ng of RNA RIN ≥ 7.0 in a 5 μl volume was used for library preparation and RNA sequencing RNAseq. Paired end sequencing libraries were prepared using the TruSeq Stranded Total Sample Preparation kit Illumina by the Mayo Clinic sequencing core facilities Rochester MN followed by quality control cluster generation and sequencing on the Illumina HiSeq 2000 platform. The reads were de multiplexed and converted to FASTQ format using CASAVA software from Illumina by the Mayo Clinic core.	GEO Accession:GSM3768989	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198600	MYCN_gas7mut_1_R2.fastq.gz MYCN_gas7mut_1_R1.fastq.gz	fastq fastq	8248008450.0	40831725.0	GSM3768989 r1	0:101 1:101	A:2002939014;C:2106228626;G:2127023982;T:2007311533;N:4505295	101	101	2002939014	2106228626	2127023982	2007311533	4505295	SRX5843740	SRS4768672	SRA887417	GEO	Mayo Clinic	2	0.80606	0.81166	0.26778	0.26818	0.72109	0.72135	0.5427	0.54592	101	101	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	trueseq	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
52263	52263	SRR9070361	SRX5846428	SRS4772046	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R165	GSM3770597	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R165	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770597	GSM3770597: EGFP oe R165; Danio rerio; RNA Seq	GSM3770597		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770597	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R165.L001_R1.fastq.gz EGFP_oe_R165.L001_R2.fastq.gz	fastq fastq	3076610200.0	15383051.0	GSM3770597 r1	0:100 1:100	A:796769616;C:732509940;G:746291003;T:799487857;N:1551784	100	100	796769616	732509940	746291003	799487857	1551784	SRX5846428	SRS4772046	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.89789	0.90025	0.23187	0.23394	0.72054	0.72914	0.49446	0.49563	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52264	52264	SRR9070362	SRX5846428	SRS4772046	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R165	GSM3770597	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R165	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770597	GSM3770597: EGFP oe R165; Danio rerio; RNA Seq	GSM3770597		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770597	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R165.L002_R1.fastq.gz EGFP_oe_R165.L002_R2.fastq.gz	fastq fastq	3086197200.0	15430986.0	GSM3770597 r2	0:100 1:100	A:799938324;C:734747735;G:748062404;T:802632934;N:815803	100	100	799938324	734747735	748062404	802632934	815803	SRX5846428	SRS4772046	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.89887	0.90081	0.23176	0.23262	0.7204	0.72805	0.49093	0.49789	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52265	52265	SRR9070359	SRX5846427	SRS4772045	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R160	GSM3770596	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R160	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770596	GSM3770596: CDK13 R860Q oe R160; Danio rerio; RNA Seq	GSM3770596		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770596	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R160.L001_R1.fastq.gz CDK13_R860Q_oe_R160.L001_R2.fastq.gz	fastq fastq	2678770600.0	13393853.0	GSM3770596 r1	0:100 1:100	A:619003093;C:719249623;G:727338824;T:611848801;N:1330259	100	100	619003093	719249623	727338824	611848801	1330259	SRX5846427	SRS4772045	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94125	0.94048	0.19284	0.20048	0.79644	0.80397	0.62455	0.62265	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52266	52266	SRR9070360	SRX5846427	SRS4772045	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R160	GSM3770596	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R160	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770596	GSM3770596: CDK13 R860Q oe R160; Danio rerio; RNA Seq	GSM3770596		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770596	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R160.L002_R1.fastq.gz CDK13_R860Q_oe_R160.L002_R2.fastq.gz	fastq fastq	2693583400.0	13467917.0	GSM3770596 r2	0:100 1:100	A:622749897;C:723537232;G:731266414;T:615327852;N:702005	100	100	622749897	723537232	731266414	615327852	702005	SRX5846427	SRS4772045	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.9417	0.9413	0.19174	0.19923	0.7921	0.80062	0.62351	0.62723	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52267	52267	SRR9070357	SRX5846426	SRS4772044	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R161	GSM3770595	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R161	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770595	GSM3770595: CDK13 R860Q oe R161; Danio rerio; RNA Seq	GSM3770595		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770595	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R161.L001_R2.fastq.gz CDK13_R860Q_oe_R161.L001_R1.fastq.gz	fastq fastq	2519068200.0	12595341.0	GSM3770595 r1	0:100 1:100	A:583021128;C:674785225;G:681628903;T:578362129;N:1270815	100	100	583021128	674785225	681628903	578362129	1270815	SRX5846426	SRS4772044	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94911	0.9495	0.18704	0.19367	0.78971	0.79555	0.60812	0.60963	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52268	52268	SRR9070358	SRX5846426	SRS4772044	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R161	GSM3770595	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R161	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770595	GSM3770595: CDK13 R860Q oe R161; Danio rerio; RNA Seq	GSM3770595		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770595	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R161.L002_R1.fastq.gz CDK13_R860Q_oe_R161.L002_R2.fastq.gz	fastq fastq	2530033400.0	12650167.0	GSM3770595 r2	0:100 1:100	A:585770003;C:678037650;G:684581661;T:580984093;N:659993	100	100	585770003	678037650	684581661	580984093	659993	SRX5846426	SRS4772044	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94949	0.94869	0.18691	0.19287	0.78904	0.79423	0.60989	0.60787	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52269	52269	SRR9070383	SRX5846425	SRS4772043	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R159	GSM3770608	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R159	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770608	GSM3770608: CDK13 R860Q oe R159; Danio rerio; RNA Seq	GSM3770608		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770608	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R159.L001_R1.fastq.gz CDK13_R860Q_oe_R159.L001_R2.fastq.gz	fastq fastq	2474506200.0	12372531.0	GSM3770608 r1	0:100 1:100	A:571838531;C:662884074;G:668025271;T:570526012;N:1232312	100	100	571838531	662884074	668025271	570526012	1232312	SRX5846425	SRS4772043	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.9432	0.94226	0.19666	0.20251	0.78748	0.79498	0.61522	0.63143	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52270	52270	SRR9070384	SRX5846425	SRS4772043	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R159	GSM3770608	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R159	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770608	GSM3770608: CDK13 R860Q oe R159; Danio rerio; RNA Seq	GSM3770608		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770608	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R159.L002_R1.fastq.gz CDK13_R860Q_oe_R159.L002_R2.fastq.gz	fastq fastq	2488931400.0	12444657.0	GSM3770608 r2	0:100 1:100	A:575442427;C:667013703;G:671842360;T:573980795;N:652115	100	100	575442427	667013703	671842360	573980795	652115	SRX5846425	SRS4772043	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94385	0.94317	0.1983	0.20419	0.78624	0.79474	0.61268	0.62588	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52271	52271	SRR9070379	SRX5846423	SRS4772041	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R158	GSM3770606	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R158	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770606	GSM3770606: CDK13 R860Q oe R158; Danio rerio; RNA Seq	GSM3770606		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770606	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R158.L001_R1.fastq.gz CDK13_R860Q_oe_R158.L001_R2.fastq.gz	fastq fastq	2825434800.0	14127174.0	GSM3770606 r1	0:100 1:100	A:677238441;C:734523392;G:737337121;T:674917300;N:1418546	100	100	677238441	734523392	737337121	674917300	1418546	SRX5846423	SRS4772041	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94498	0.94425	0.18907	0.19315	0.778	0.78246	0.57411	0.59623	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52272	52272	SRR9070380	SRX5846423	SRS4772041	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R158	GSM3770606	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R158	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770606	GSM3770606: CDK13 R860Q oe R158; Danio rerio; RNA Seq	GSM3770606		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770606	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R158.L002_R1.fastq.gz CDK13_R860Q_oe_R158.L002_R2.fastq.gz	fastq fastq	2843101200.0	14215506.0	GSM3770606 r2	0:100 1:100	A:681805847;C:739425518;G:741775554;T:679334464;N:759817	100	100	681805847	739425518	741775554	679334464	759817	SRX5846423	SRS4772041	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.94583	0.94538	0.19056	0.19593	0.77429	0.77983	0.58126	0.59795	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52273	52273	SRR9070369	SRX5846418	SRS4772036	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R157	GSM3770601	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R157	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770601	GSM3770601: CDK13 R860Q oe R157; Danio rerio; RNA Seq	GSM3770601		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770601	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R157.L001_R1.fastq.gz CDK13_R860Q_oe_R157.L001_R2.fastq.gz	fastq fastq	3661632000.0	18308160.0	GSM3770601 r1	0:100 1:100	A:922608217;C:907144149;G:904156678;T:925925771;N:1797185	100	100	922608217	907144149	904156678	925925771	1797185	SRX5846418	SRS4772036	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.74235	0.73621	0.13938	0.14183	0.77173	0.7811	0.48933	0.55655	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52274	52274	SRR9070370	SRX5846418	SRS4772036	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		CDK13 R860Q oe R157	GSM3770601	source name:Melanoma\|tissue:Melanoma\|cdk13 status:R860Q	CDK13 R860Q oe R157	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:R860Q	GSM3770601	GSM3770601: CDK13 R860Q oe R157; Danio rerio; RNA Seq	GSM3770601		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770601	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	CDK13_R860Q_oe_R157.L002_R1.fastq.gz CDK13_R860Q_oe_R157.L002_R2.fastq.gz	fastq fastq	3665362400.0	18326812.0	GSM3770601 r2	0:100 1:100	A:924047293;C:908396365;G:904889672;T:927121273;N:907797	100	100	924047293	908396365	904889672	927121273	907797	SRX5846418	SRS4772036	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.74534	0.73923	0.13944	0.14274	0.77222	0.78011	0.47479	0.5489	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52275	52275	SRR9070367	SRX5846417	SRS4772035	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R162	GSM3770600	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R162	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770600	GSM3770600: EGFP oe R162; Danio rerio; RNA Seq	GSM3770600		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770600	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R162.L001_R1.fastq.gz EGFP_oe_R162.L001_R2.fastq.gz	fastq fastq	2656608000.0	13283040.0	GSM3770600 r1	0:100 1:100	A:588214152;C:738647621;G:741202972;T:587227120;N:1316135	100	100	588214152	738647621	741202972	587227120	1316135	SRX5846417	SRS4772035	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.96224	0.96157	0.19778	0.20061	0.83069	0.83711	0.64663	0.66048	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52276	52276	SRR9070368	SRX5846417	SRS4772035	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R162	GSM3770600	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R162	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770600	GSM3770600: EGFP oe R162; Danio rerio; RNA Seq	GSM3770600		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770600	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R162.L002_R1.fastq.gz EGFP_oe_R162.L002_R2.fastq.gz	fastq fastq	2677422400.0	13387112.0	GSM3770600 r2	0:100 1:100	A:592938070;C:744912021;G:747019801;T:591841669;N:710839	100	100	592938070	744912021	747019801	591841669	710839	SRX5846417	SRS4772035	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.96179	0.96197	0.19784	0.2032	0.83189	0.83857	0.65734	0.65329	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52277	52277	SRR9070365	SRX5846416	SRS4772034	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R163	GSM3770599	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R163	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770599	GSM3770599: EGFP oe R163; Danio rerio; RNA Seq	GSM3770599		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770599	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R163.L001_R2.fastq.gz EGFP_oe_R163.L001_R1.fastq.gz	fastq fastq	2200167400.0	11000837.0	GSM3770599 r1	0:100 1:100	A:557687138;C:532009113;G:541257695;T:568085676;N:1127778	100	100	557687138	532009113	541257695	568085676	1127778	SRX5846416	SRS4772034	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.91699	0.91547	0.25451	0.25122	0.74197	0.74866	0.49383	0.48521	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52278	52278	SRR9070366	SRX5846416	SRS4772034	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R163	GSM3770599	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R163	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770599	GSM3770599: EGFP oe R163; Danio rerio; RNA Seq	GSM3770599		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770599	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R163.L002_R2.fastq.gz EGFP_oe_R163.L002_R1.fastq.gz	fastq fastq	2207341000.0	11036705.0	GSM3770599 r2	0:100 1:100	A:560113696;C:533571442;G:542576508;T:570500106;N:579248	100	100	560113696	533571442	542576508	570500106	579248	SRX5846416	SRS4772034	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.91607	0.91622	0.24532	0.25042	0.74245	0.75014	0.49012	0.48115	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52279	52279	SRR9070363	SRX5846415	SRS4772033	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R164	GSM3770598	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R164	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770598	GSM3770598: EGFP oe R164; Danio rerio; RNA Seq	GSM3770598		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770598	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R164.L001_R1.fastq.gz EGFP_oe_R164.L001_R2.fastq.gz	fastq fastq	2526684200.0	12633421.0	GSM3770598 r1	0:100 1:100	A:560721104;C:699940935;G:697771716;T:566983213;N:1267232	100	100	560721104	699940935	697771716	566983213	1267232	SRX5846415	SRS4772033	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.95624	0.9564	0.18619	0.18787	0.79082	0.79766	0.66256	0.66357	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
52280	52280	SRR9070364	SRX5846415	SRS4772033	SRP198646	PRJNA543299	Oncogenic CDK13 Mutations Impede Nuclear RNA Surveillance zfRNAseq	GSE131333	Transcriptome Analysis	RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We find disrupted nuclear RNA surveillance is oncogenic. Cyclin Dependent Kinase 13 CDK13 is mutated in melanoma and patient mutated CDK13 accelerates zebrafish melanoma. CDK13 mutation causes aberrant RNA stabilization. CDK13 is required for ZC3H14 phosphorylation which is necessary and sufficient to promote nuclear RNA degradation. Mutant CDK13 fails to activate nuclear RNA surveillance causing aberrant protein coding transcripts to be stabilized and translated. Forced aberrant RNA expression accelerates melanoma in zebrafish. We find recurrent mutations in genes encoding nuclear RNA surveillance components in many malignancies establishing nuclear RNA surveillance as a tumor suppressive pathway. Activating nuclear RNA surveillance is crucial to avoid accumulation of aberrant RNAs and their ensuing consequences in development and disease. Overall design: RNA Seq in zebrafish melanoma expressing EGFP or mutant CDK13	parent bioproject:PRJNA543289		EGFP oe R164	GSM3770598	source name:Melanoma\|tissue:Melanoma\|cdk13 status:Wild type	EGFP oe R164	Reads were aligned to a custom version of the danRer10 genome that also contained the human CDK13 gene sequence using bowtie with parameters library type fr unstranded no novel juncs and G set revision 90 of the Ensembl GRCz10 genes Expression of revision 90 GRCz10 genes was quantified using htseq count with parameters r name I gene name stranded=no m intersection strict Supplementary files format and content: Counts files contain gene names and htseq determined read counts	Melanoma		Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	p53 / ; mitfa:BRAFV600E;Na / one cell embryos were injected with either 20ng/uL control or experimental MiniCoopR MCR DNA along with tol2 in vitro transcribed RNA for integration. In all experiments 20 zebrafish were raised per tank to control for density effects. Zebrafish were scored for the emergence of raised melanoma lesions as published. Zebrafish were sacrificed on ice and the tumors were dissected.	tissue:Melanoma\|cdk13 status:Wild type	GSM3770598	GSM3770598: EGFP oe R164; Danio rerio; RNA Seq	GSM3770598		1	Library prepped with random priming NEBNext Ultra RNA Library Prep Kit for Illumina E7530 fragmentation time of 15min 12 PCR cycles and sequenced on an Illumina HiSeq 2000 100bp paired end reads. Melanomas were homogenized in RLT buffer subjected to QIAshredder columns Qiagen 79656 and then RNA was isolated with a column based method with genomic DNA column removal Qiagen 74134. RNA was ribodepleted Illumina Ribozero Gold MRZG12324. Ribodepletion was confirmed with Agilent 4200 Tapestation.	GEO Accession:GSM3770598	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP198646	EGFP_oe_R164.L002_R1.fastq.gz EGFP_oe_R164.L002_R2.fastq.gz	fastq fastq	2537225800.0	12686129.0	GSM3770598 r2	0:100 1:100	A:563232695;C:703247791;G:700738652;T:569350993;N:655669	100	100	563232695	703247791	700738652	569350993	655669	SRX5846415	SRS4772033	SRA887503	GEO	Young Lab, Whitehead Institute for Biomedical Research	2	0.95722	0.95739	0.18563	0.18908	0.79155	0.7989	0.66665	0.66441	100	100	B	B	biological fallback assumption	illumina	hiseq_era	unknown	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-05-16	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53570	53570	SRR9944760	SRX6693259	SRS5250599	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	myrAKT#4	GSM4026007	tissue:Zebrafish gangli1uroma tumor cells\|genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	myrAKT#4	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish ganglioneuroma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	GSM4026007	GSM4026007: myrAKT#4; Danio rerio; RNA Seq	GSM4026007		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	myrAKT_4_R1_001.fastq.gz myrAKT_4_R2_001.fastq.gz	fastq fastq	8224461750.0	54829745.0	GSM4026007 r1	0:75 1:75	A:2181296095;C:1913052498;G:1987660432;T:2140385772;N:2066953	75	75	2181296095	1913052498	1987660432	2140385772	2066953	SRX6693259	SRS5250599	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.94834	0.95102	0.09336	0.09188	0.71366	0.71528	0.56498	0.56601	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53571	53571	SRR9944759	SRX6693258	SRS5250598	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	myrAKT#3	GSM4026006	tissue:Zebrafish gangli1uroma tumor cells\|genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	myrAKT#3	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish ganglioneuroma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	GSM4026006	GSM4026006: myrAKT#3; Danio rerio; RNA Seq	GSM4026006		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	myrAKT_3_R1_001.fastq.gz myrAKT_3_R2_001.fastq.gz	fastq fastq	11540448600.0	76936324.0	GSM4026006 r1	0:75 1:75	A:3012275404;C:2726671725;G:2851855990;T:2946734338;N:2911143	75	75	3012275404	2726671725	2851855990	2946734338	2911143	SRX6693258	SRS5250598	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.95135	0.92555	0.08121	0.07749	0.71796	0.72401	0.56751	0.57038	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53572	53572	SRR9944758	SRX6693257	SRS5250597	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	myrAKT#2	GSM4026005	tissue:Zebrafish gangli1uroma tumor cells\|genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	myrAKT#2	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish ganglioneuroma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	GSM4026005	GSM4026005: myrAKT#2; Danio rerio; RNA Seq	GSM4026005		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	myrAKT_2_R1_001.fastq.gz myrAKT_2_R2_001.fastq.gz	fastq fastq	12386608800.0	82577392.0	GSM4026005 r1	0:75 1:75	A:3216847372;C:2944029674;G:3084994278;T:3137609686;N:3127790	75	75	3216847372	2944029674	3084994278	3137609686	3127790	SRX6693257	SRS5250597	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.94942	0.95273	0.09002	0.08825	0.72232	0.72527	0.52131	0.52677	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53573	53573	SRR9944757	SRX6693256	SRS5250596	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	myrAKT#1	GSM4026004	tissue:Zebrafish gangli1uroma tumor cells\|genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	myrAKT#1	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish ganglioneuroma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:myrAKT transgenic fish\|cell type:gangli1uroma cells	GSM4026004	GSM4026004: myrAKT#1; Danio rerio; RNA Seq	GSM4026004		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	myrAKT_1_R2_001.fastq.gz myrAKT_1_R1_001.fastq.gz	fastq fastq	10533443400.0	70222956.0	GSM4026004 r1	0:75 1:75	A:2713017255;C:2528083140;G:2625072686;T:2664616663;N:2653656	75	75	2713017255	2528083140	2625072686	2664616663	2653656	SRX6693256	SRS5250596	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.95384	0.95698	0.0792	0.07709	0.7249	0.72711	0.53397	0.53326	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53574	53574	SRR9944756	SRX6693255	SRS5250595	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	MYCN#4	GSM4026003	tissue:Zebrafish neuroblastoma tumor cells\|genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	MYCN#4	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish neuroblastoma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	GSM4026003	GSM4026003: MYCN#4; Danio rerio; RNA Seq	GSM4026003		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	MYCN_4_R1_001.fastq.gz MYCN_4_R2_001.fastq.gz	fastq fastq	12647410500.0	84316070.0	GSM4026003 r1	0:75 1:75	A:3192174853;C:3078742090;G:3255144371;T:3118165180;N:3184006	75	75	3192174853	3078742090	3255144371	3118165180	3184006	SRX6693255	SRS5250595	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.9678	0.96946	0.04813	0.0467	0.7553	0.75972	0.54218	0.53492	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53575	53575	SRR9944755	SRX6693254	SRS5250594	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	MYCN#3	GSM4026002	tissue:Zebrafish neuroblastoma tumor cells\|genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	MYCN#3	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish neuroblastoma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	GSM4026002	GSM4026002: MYCN#3; Danio rerio; RNA Seq	GSM4026002		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	MYCN_3_R1_001.fastq.gz MYCN_3_R2_001.fastq.gz	fastq fastq	10429575150.0	69530501.0	GSM4026002 r1	0:75 1:75	A:2736293587;C:2459385850;G:2579079974;T:2654428416;N:387323	75	75	2736293587	2459385850	2579079974	2654428416	387323	SRX6693254	SRS5250594	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.95299	0.95438	0.08493	0.08121	0.73399	0.74432	0.51135	0.52439	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53576	53576	SRR9944754	SRX6693253	SRS5250593	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	MYCN#2	GSM4026001	tissue:Zebrafish neuroblastoma tumor cells\|genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	MYCN#2	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish neuroblastoma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	GSM4026001	GSM4026001: MYCN#2; Danio rerio; RNA Seq	GSM4026001		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	MYCN_2_R1_001.fastq.gz MYCN_2_R2_001.fastq.gz	fastq fastq	9518711400.0	63458076.0	GSM4026001 r1	0:75 1:75	A:2440261186;C:2291125181;G:2425125263;T:2361842692;N:357078	75	75	2440261186	2291125181	2425125263	2361842692	357078	SRX6693253	SRS5250593	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.95917	0.96071	0.07229	0.06951	0.74586	0.75666	0.5264	0.51949	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
53577	53577	SRR9944753	SRX6693252	SRS5250592	SRP218009	PRJNA559652	Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors	GSE135682	Transcriptome Analysis	Peripheral sympathetic nervous system tumors are the most common extra cranial pediatric tumors in children and include neuroblastoma ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto oncogene or activated Ras in murine models but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas but only in a small portion of human poorly differentiated neuroblastomas p<0.0001 Fisher's exact test. As a result we created zebrafish transgenic for constitutively activated myr Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without xxx to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets phosphorylated mTOR S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target mTOR using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma and propose inhibition of the AKT target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma. Overall design: RNA Seq for zebrafish tumor cells from MYCN and myrAKT transgenic fish		pubmed:32728700	MYCN#1	GSM4026000	tissue:Zebrafish neuroblastoma tumor cells\|genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	MYCN#1	post acquiring the raw fastq format paired end RNA seq reads we inspected the sequencing quality using fastqc v0.11.5 and removed standard Illumina adapters from the 3’ end using Trim Galore v0.4.4. The processed reads were then aligned to the GRCz10 version of the zebrafish reference genome using Tophat v2.1.1. The GTF format UCSC gene models obtained from the iGenomes website was provided as an annotation reference G option of Tophat. post the alignment the BAM format files were sorted by reads name using Samtools v1.5 and the reads mapped to each gene were counted using HTSeq count v0.6.1. edgeR library was applied to normalize read counts across samples and identify genes that are differentially expressed between conditions in R. Genome build: GRCz10 Supplementary files format and content: counts	Zebrafish neuroblastoma tumor cells	None	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer’s protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.	EGFP+ neuroblastoma cells or mCherry+ ganglioneuroma cells were harvested from tumor bearing MYCN or myrAkt transgenic zebrafish. Tumors were mechanically homogenized and EGFP+ or mCherry+ cells were sorted directly into Trizol LS	genotype/variation:MYCN transgenic fish\|cell type:neuroblastoma cells	GSM4026000	GSM4026000: MYCN#1; Danio rerio; RNA Seq	GSM4026000		1	EGFP+ or mCherry+ tumor cells were sorted then total RNA was extracted with Trizol LS. Total RNA was depleted of ribosomal RNA with the SMARTer Universal Low Input RNA Kit Clontech. Enriched mRNA was then applied to library preparation according to manufacturer's protocol NEBNext Ultra. post repeated quality control for average DNA input size of 300 bp the samples were sequenced on aIllumina NextSeq 500 with 2X75bp paired end reads.		RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 500	SRP218009	MYCN_1_R1_001.fastq.gz MYCN_1_R2_001.fastq.gz	fastq fastq	12249512250.0	81663415.0	GSM4026000 r1	0:75 1:75	A:3146759551;C:2963459721;G:3078804965;T:3060035031;N:452982	75	75	3146759551	2963459721	3078804965	3060035031	452982	SRX6693252	SRS5250592	SRA937501	GEO	Thomas Look, Pediatric Oncology, Dana-Farber Cancer Institute	2	0.95937	0.95322	0.06466	0.06119	0.7484	0.76071	0.51653	0.51684	75	75	B	B	biological fallback assumption	illumina	nextseq	full_length	rrna_depletion	nebnext	bulk	unknown	unknown	United States	2019-08-10	Undetermined	Embryo	Cancer or Tumor	Cancer or Tumor
56354	56354	SRR10956577	SRX7622793	SRS6054747	SRP244262	PRJNA602818	Oxidative phosphorylation promotes primary melanoma invasion	GSE144117	Transcriptome Analysis	Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively whereas the early progression of non invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth the first step in melanoma invasion we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 RSK1 drives tumor invasion. Transcriptomic analysis of RSK1 activated tumors identified metabolic changes including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator activated receptor gamma coactivator 1a PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki 67 and the reactive oxygen species ROS scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion including oxidative stress. Our results support a role for PGC1a in mediating glutamine driven OXPHOS to facilitate the invasive growth of primary melanoma. Overall design: Melanomas harvested from MiniCoopR GFP zebrafish n=6 and MiniCoopR myrRSK n=6 zebrafish		pubmed:32142731	MiniCoopR MyrRSK melanoma rep6	GSM4280518	source name:MiniCoopR MyrRSK melanoma\|genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	MiniCoopR MyrRSK melanoma rep6	Reads were aligned using STAR v2.6.1d Dobin A Davis CA Schlesinger F Drenkow J Zaleski C Jha S Batut P Chaisson M Gingeras TR: STAR: ultrafast universal RNA seq aligner. Bioinformatics Oxford England 2013 29:15 21. Read counting was performed using htseq count v0.6.0 Differential gene expression was performed using Deseq2 Love MI Huber W Anders S: Moderated estimation of fold change and dispersion for RNA seq data with DESeq2. Genome biology 2014 15:550. Genome build: Zv9 Supplementary files format and content: Differential gene expression was performed using Deseq2 and outputted in a .csv file with ensembl gene identifiers.	MiniCoopR MyrRSK melanoma	None	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	Routine zebrafish husbandry	genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	GSM4280518	GSM4280518: MiniCoopR MyrRSK melanoma rep6; Danio rerio; RNA Seq	GSM4280518		1	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	GEO Accession:GSM4280518	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP244262	MC_MYR6_R1.fastq.gz MC_MYR6_R2.fastq.gz	fastq fastq	3885154602.0	38089751.0	GSM4280518 r1	0:51 1:51	A:1041821822;C:906528243;G:889670641;T:1043891035;N:3242861	51	51	1041821822	906528243	889670641	1043891035	3242861	SRX7622793	SRS6054747	SRA1030535	GEO	Surgery, Weill Cornell Medical College	2	0.92435	0.92643	0.0979	0.09909	0.71581	0.71579	0.49527	0.50224	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-01-23	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
56355	56355	SRR10956576	SRX7622792	SRS6054746	SRP244262	PRJNA602818	Oxidative phosphorylation promotes primary melanoma invasion	GSE144117	Transcriptome Analysis	Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively whereas the early progression of non invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth the first step in melanoma invasion we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 RSK1 drives tumor invasion. Transcriptomic analysis of RSK1 activated tumors identified metabolic changes including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator activated receptor gamma coactivator 1a PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki 67 and the reactive oxygen species ROS scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion including oxidative stress. Our results support a role for PGC1a in mediating glutamine driven OXPHOS to facilitate the invasive growth of primary melanoma. Overall design: Melanomas harvested from MiniCoopR GFP zebrafish n=6 and MiniCoopR myrRSK n=6 zebrafish		pubmed:32142731	MiniCoopR MyrRSK melanoma rep5	GSM4280517	source name:MiniCoopR MyrRSK melanoma\|genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	MiniCoopR MyrRSK melanoma rep5	Reads were aligned using STAR v2.6.1d Dobin A Davis CA Schlesinger F Drenkow J Zaleski C Jha S Batut P Chaisson M Gingeras TR: STAR: ultrafast universal RNA seq aligner. Bioinformatics Oxford England 2013 29:15 21. Read counting was performed using htseq count v0.6.0 Differential gene expression was performed using Deseq2 Love MI Huber W Anders S: Moderated estimation of fold change and dispersion for RNA seq data with DESeq2. Genome biology 2014 15:550. Genome build: Zv9 Supplementary files format and content: Differential gene expression was performed using Deseq2 and outputted in a .csv file with ensembl gene identifiers.	MiniCoopR MyrRSK melanoma	None	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	Routine zebrafish husbandry	genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	GSM4280517	GSM4280517: MiniCoopR MyrRSK melanoma rep5; Danio rerio; RNA Seq	GSM4280517		1	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	GEO Accession:GSM4280517	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP244262	MC_MYR5_R1.fastq.gz MC_MYR5_R2.fastq.gz	fastq fastq	3676332042.0	36042471.0	GSM4280517 r1	0:51 1:51	A:985224956;C:859001351;G:842223276;T:986780285;N:3102174	51	51	985224956	859001351	842223276	986780285	3102174	SRX7622792	SRS6054746	SRA1030535	GEO	Surgery, Weill Cornell Medical College	2	0.92186	0.92546	0.10291	0.10427	0.71415	0.71569	0.50935	0.50965	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-01-23	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
56356	56356	SRR10956575	SRX7622791	SRS6054745	SRP244262	PRJNA602818	Oxidative phosphorylation promotes primary melanoma invasion	GSE144117	Transcriptome Analysis	Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively whereas the early progression of non invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth the first step in melanoma invasion we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 RSK1 drives tumor invasion. Transcriptomic analysis of RSK1 activated tumors identified metabolic changes including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator activated receptor gamma coactivator 1a PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki 67 and the reactive oxygen species ROS scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion including oxidative stress. Our results support a role for PGC1a in mediating glutamine driven OXPHOS to facilitate the invasive growth of primary melanoma. Overall design: Melanomas harvested from MiniCoopR GFP zebrafish n=6 and MiniCoopR myrRSK n=6 zebrafish		pubmed:32142731	MiniCoopR MyrRSK melanoma rep4	GSM4280516	source name:MiniCoopR MyrRSK melanoma\|genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	MiniCoopR MyrRSK melanoma rep4	Reads were aligned using STAR v2.6.1d Dobin A Davis CA Schlesinger F Drenkow J Zaleski C Jha S Batut P Chaisson M Gingeras TR: STAR: ultrafast universal RNA seq aligner. Bioinformatics Oxford England 2013 29:15 21. Read counting was performed using htseq count v0.6.0 Differential gene expression was performed using Deseq2 Love MI Huber W Anders S: Moderated estimation of fold change and dispersion for RNA seq data with DESeq2. Genome biology 2014 15:550. Genome build: Zv9 Supplementary files format and content: Differential gene expression was performed using Deseq2 and outputted in a .csv file with ensembl gene identifiers.	MiniCoopR MyrRSK melanoma	None	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	Routine zebrafish husbandry	genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	GSM4280516	GSM4280516: MiniCoopR MyrRSK melanoma rep4; Danio rerio; RNA Seq	GSM4280516		1	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	GEO Accession:GSM4280516	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP244262	MC_MYR4_R1.fastq.gz MC_MYR4_R2.fastq.gz	fastq fastq	3784545576.0	37103388.0	GSM4280516 r1	0:51 1:51	A:1013258781;C:883885770;G:869960057;T:1014261768;N:3179200	51	51	1013258781	883885770	869960057	1014261768	3179200	SRX7622791	SRS6054745	SRA1030535	GEO	Surgery, Weill Cornell Medical College	2	0.91884	0.92251	0.08776	0.08979	0.72391	0.72521	0.51279	0.50988	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-01-23	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
56357	56357	SRR10956574	SRX7622790	SRS6054744	SRP244262	PRJNA602818	Oxidative phosphorylation promotes primary melanoma invasion	GSE144117	Transcriptome Analysis	Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively whereas the early progression of non invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth the first step in melanoma invasion we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 RSK1 drives tumor invasion. Transcriptomic analysis of RSK1 activated tumors identified metabolic changes including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator activated receptor gamma coactivator 1a PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki 67 and the reactive oxygen species ROS scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion including oxidative stress. Our results support a role for PGC1a in mediating glutamine driven OXPHOS to facilitate the invasive growth of primary melanoma. Overall design: Melanomas harvested from MiniCoopR GFP zebrafish n=6 and MiniCoopR myrRSK n=6 zebrafish		pubmed:32142731	MiniCoopR MyrRSK melanoma rep3	GSM4280515	source name:MiniCoopR MyrRSK melanoma\|genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	MiniCoopR MyrRSK melanoma rep3	Reads were aligned using STAR v2.6.1d Dobin A Davis CA Schlesinger F Drenkow J Zaleski C Jha S Batut P Chaisson M Gingeras TR: STAR: ultrafast universal RNA seq aligner. Bioinformatics Oxford England 2013 29:15 21. Read counting was performed using htseq count v0.6.0 Differential gene expression was performed using Deseq2 Love MI Huber W Anders S: Moderated estimation of fold change and dispersion for RNA seq data with DESeq2. Genome biology 2014 15:550. Genome build: Zv9 Supplementary files format and content: Differential gene expression was performed using Deseq2 and outputted in a .csv file with ensembl gene identifiers.	MiniCoopR MyrRSK melanoma	None	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	Routine zebrafish husbandry	genotype:MiniCoopR MyrRSK\|tissue:zebrafish melanoma	GSM4280515	GSM4280515: MiniCoopR MyrRSK melanoma rep3; Danio rerio; RNA Seq	GSM4280515		1	Total RNA was isolated using Rneasy plus mini kit Qiagen according to the manufacturer's protocol Library construction was performed using Illumina reagents according to the manufacturer's protocol	GEO Accession:GSM4280515	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina HiSeq 2000	SRP244262	MC_MYR3_R1.fastq.gz MC_MYR3_R2.fastq.gz	fastq fastq	3623906286.0	35528493.0	GSM4280515 r1	0:51 1:51	A:978261360;C:838748259;G:823759467;T:980072429;N:3064771	51	51	978261360	838748259	823759467	980072429	3064771	SRX7622790	SRS6054744	SRA1030535	GEO	Surgery, Weill Cornell Medical College	2	0.91411	0.91459	0.11142	0.11256	0.70376	0.70463	0.49684	0.49632	51	51	B	B	biological fallback assumption	illumina	hiseq_era	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	United States	2020-01-23	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor

Advanced export

JSON shape: default, array, newline-delimited

CREATE TABLE run_metadata("run.accession" VARCHAR, "experiment.accession" VARCHAR, "sample.accession" VARCHAR, "study.accession" VARCHAR, bioproject VARCHAR, "study.title" VARCHAR, "study.alias" VARCHAR, "study.type" VARCHAR, "study.abstract" VARCHAR, "study.attributes" VARCHAR, "study.PMIDs" VARCHAR, "sample.description" VARCHAR, "sample.title" VARCHAR, "sample.alias" VARCHAR, "sample.centername" VARCHAR, "sample.attributes" VARCHAR, "GEOsample.title" VARCHAR, "GEOsample.dataprocessing" VARCHAR, "GEOsample.source" VARCHAR, "GEOsample.treatmentprotocol" VARCHAR, "GEOsample.extractprotocol" VARCHAR, "GEOsample.growthprotocol" VARCHAR, "GEOsample.characteristics" VARCHAR, "GEOsample.accession" VARCHAR, "experiment.title" VARCHAR, "experiment.alias" VARCHAR, "experiment.library_name" VARCHAR, "experiment.design_description" VARCHAR, "experiment.library_construction_protocol" VARCHAR, "experiment.attributes" VARCHAR, "experiment.library_strategy" VARCHAR, "experiment.library_source" VARCHAR, "experiment.library_selection" VARCHAR, "experiment.library_layout" VARCHAR, "experiment.platform" VARCHAR, "experiment.instrument_model" VARCHAR, "experiment.spot_descriptor" VARCHAR, "experiment.study_ref" VARCHAR, "run.title" VARCHAR, "run.attributes" VARCHAR, "run.filename" VARCHAR, "run.semantic_name" VARCHAR, "run.total_bases" DOUBLE, "run.total_spots" DOUBLE, "run.alias" VARCHAR, "run.read_lengths" VARCHAR, "run.base_counts" VARCHAR, "run.r1_length" BIGINT, "run.r2_length" BIGINT, "run.r3_length" BIGINT, "run.r4_length" BIGINT, "run.Acount" BIGINT, "run.Ccount" BIGINT, "run.Gcount" BIGINT, "run.Tcount" BIGINT, "run.Ncount" BIGINT, "run.experiment" VARCHAR, "run.pool_member" VARCHAR, "submission.accession" VARCHAR, "submission.srasource" VARCHAR, "submission.bioprojectsource" VARCHAR, "seqdetective.n_mates" BIGINT, "seqdetective.mapping_rate.mate1" DOUBLE, "seqdetective.mapping_rate.mate2" DOUBLE, "seqdetective.nofeature_rate.mate1" DOUBLE, "seqdetective.nofeature_rate.mate2" DOUBLE, "seqdetective.sparsity.mate1" DOUBLE, "seqdetective.sparsity.mate2" DOUBLE, "seqdetective.pos_strand_rate.mate1" DOUBLE, "seqdetective.pos_strand_rate.mate2" DOUBLE, "seqdetective.readlen.mate1" BIGINT, "seqdetective.readlen.mate2" BIGINT, "seqdetective.judgement.mate1" VARCHAR, "seqdetective.judgement.mate2" VARCHAR, "seqdetective.judgement.reason" VARCHAR, platform_family VARCHAR, instrument_generation VARCHAR, read_bias VARCHAR, selection_class VARCHAR, prep_kit VARCHAR, sc_or_bulk VARCHAR, tech_class VARCHAR, technology VARCHAR, tech_variant VARCHAR, "submission.bioprojectsource.country" VARCHAR, earliest_date DATE, devstage_curation VARCHAR, devstage_curation_coarse VARCHAR, tissue_curation VARCHAR, tissue_curation_coarse VARCHAR);;
CREATE INDEX idx_run_bioproject ON run_metadata(bioproject);;
CREATE INDEX idx_run_run_accession ON run_metadata("run.accession");;