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327 rows where technology = "unknown" and tissue_curation = "Cancer or Tumor"

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  • Cancer or Tumor · 327 ✖

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  • unknown · 327 ✖

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Link rowid ▼ run.accession experiment.accession sample.accession study.accession bioproject study.title study.alias study.type study.abstract study.attributes study.PMIDs sample.description sample.title sample.alias sample.centername 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.spot_descriptor experiment.study_ref run.title run.attributes 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.r3_length run.r4_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 tech_variant 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
41564 41564 SRR5044691 SRX2367699 SRS1813797 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 4 GSM2399713   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 4 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 GSM2399713 GSM2399713: ZMEL1 METASTATIC REP 4; Danio rerio; RNA Seq GSM2399713   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399713 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-A1-ISK-GFP-pos_CTTGTA_AHBENJADXX_L001_001.R1.fastq fastq 1021688450.0 20433769.0 GSM2399713 r1 0:50 A:263964434;C:226020906;G:246160135;T:285440788;N:102187 50       263964434 226020906 246160135 285440788 102187 SRX2367699 SRS1813797 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.86173   0.35054   0.78305   0.63081   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41565 41565 SRR5044692 SRX2367699 SRS1813797 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 4 GSM2399713   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 4 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 GSM2399713 GSM2399713: ZMEL1 METASTATIC REP 4; Danio rerio; RNA Seq GSM2399713   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399713 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-A1-ISK-GFP-pos_CTTGTA_AHBENJADXX_L002_001.R1.fastq fastq 948274550.0 18965491.0 GSM2399713 r2 0:50 A:244756056;C:209496504;G:228095978;T:264427260;N:1498752 50       244756056 209496504 228095978 264427260 1498752 SRX2367699 SRS1813797 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.86249   0.35012   0.78147   0.61412   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41566 41566 SRR5044689 SRX2367698 SRS1813796 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 3 GSM2399712   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 3 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 GSM2399712 GSM2399712: ZMEL1 METASTATIC REP 3; Danio rerio; RNA Seq GSM2399712   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399712 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-4-GFP-POS_AGTTCC_AHBENJADXX_L001_001.R1.fastq fastq 547347950.0 10946959.0 GSM2399712 r1 0:50 A:142532772;C:118021475;G:130457816;T:156280877;N:55010 50       142532772 118021475 130457816 156280877 55010 SRX2367698 SRS1813796 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.82238   0.37848   0.81511   0.68704   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41567 41567 SRR5044690 SRX2367698 SRS1813796 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 3 GSM2399712   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 3 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 GSM2399712 GSM2399712: ZMEL1 METASTATIC REP 3; Danio rerio; RNA Seq GSM2399712   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399712 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-4-GFP-POS_AGTTCC_AHBENJADXX_L002_001.R1.fastq fastq 507753450.0 10155069.0 GSM2399712 r2 0:50 A:132079203;C:109301536;G:120877231;T:144665731;N:829749 50       132079203 109301536 120877231 144665731 829749 SRX2367698 SRS1813796 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.8144   0.37493   0.81682   0.68224   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41568 41568 SRR5044687 SRX2367697 SRS1813798 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 2 GSM2399711   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 2 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 GSM2399711 GSM2399711: ZMEL1 METASTATIC REP 2; Danio rerio; RNA Seq GSM2399711   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399711 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-3-GFP-POS_AGTCAA_AHBENJADXX_L001_001.R1.fastq fastq 487099600.0 9741992.0 GSM2399711 r1 0:50 A:128774562;C:103935704;G:114312614;T:140027704;N:49016 50       128774562 103935704 114312614 140027704 49016 SRX2367697 SRS1813798 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.83241   0.38945   0.77759   0.63782   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41569 41569 SRR5044688 SRX2367697 SRS1813798 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 2 GSM2399711   tissue:ZMEL1 cells in vivo|cell type:ZMEL1|tissue type:melanoma ZMEL1 METASTATIC REP 2 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 GSM2399711 GSM2399711: ZMEL1 METASTATIC REP 2; Danio rerio; RNA Seq GSM2399711   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399711 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     DISSEMINATED-3-GFP-POS_AGTCAA_AHBENJADXX_L002_001.R1.fastq fastq 452003900.0 9040078.0 GSM2399711 r2 0:50 A:119365829;C:96270497;G:105927958;T:129699772;N:739844 50       119365829 96270497 105927958 129699772 739844 SRX2367697 SRS1813798 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.8334   0.39284   0.78033   0.63687   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval 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
41571 41571 SRR5044684 SRX2367695 SRS1813794 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 IN VITRO REP 2 GSM2399709   tissue:ZMEL1 cells in vitro|cell type:ZMEL1|tissue type:melanoma ZMEL1 IN VITRO REP 2 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 vitro 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 GSM2399709 GSM2399709: ZMEL1 IN VITRO REP 2; Danio rerio; RNA Seq GSM2399709   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399709 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     ZMEL3-ISK_CGATGT_AHBENJADXX_L001_001.R1.fastq fastq 769908950.0 15398179.0 GSM2399709 r1 0:50 A:182817342;C:191713397;G:197387080;T:197914424;N:76707 50       182817342 191713397 197387080 197914424 76707 SRX2367695 SRS1813794 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.90333   0.27932   0.80894   0.6691   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41572 41572 SRR5044685 SRX2367695 SRS1813794 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 IN VITRO REP 2 GSM2399709   tissue:ZMEL1 cells in vitro|cell type:ZMEL1|tissue type:melanoma ZMEL1 IN VITRO REP 2 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 vitro 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 GSM2399709 GSM2399709: ZMEL1 IN VITRO REP 2; Danio rerio; RNA Seq GSM2399709   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399709 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     ZMEL3-ISK_CGATGT_AHBENJADXX_L002_001.R1.fastq fastq 713052900.0 14261058.0 GSM2399709 r2 0:50 A:169193359;C:177235371;G:182562897;T:182889589;N:1171684 50       169193359 177235371 182562897 182889589 1171684 SRX2367695 SRS1813794 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.90483   0.2787   0.80892   0.66955   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41573 41573 SRR5044682 SRX2367694 SRS1813793 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 IN VITRO REP 1 GSM2399708   tissue:ZMEL1 cells in vitro|cell type:ZMEL1|tissue type:melanoma ZMEL1 IN VITRO 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 vitro 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 GSM2399708 GSM2399708: ZMEL1 IN VITRO REP 1; Danio rerio; RNA Seq GSM2399708   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399708 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     ZMEL1_ATCACG_AHBENJADXX_L001_001.R1.fastq fastq 480071700.0 9601434.0 GSM2399708 r1 0:50 A:126381285;C:102596587;G:111718527;T:139327539;N:47762 50       126381285 102596587 111718527 139327539 47762 SRX2367694 SRS1813793 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.86224   0.32994   0.78106   0.62148   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41574 41574 SRR5044683 SRX2367694 SRS1813793 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 IN VITRO REP 1 GSM2399708   tissue:ZMEL1 cells in vitro|cell type:ZMEL1|tissue type:melanoma ZMEL1 IN VITRO 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 vitro 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 GSM2399708 GSM2399708: ZMEL1 IN VITRO REP 1; Danio rerio; RNA Seq GSM2399708   1 Cells were FACS sorted and total RNA isolated with Zymo kits Illumina TruSeq GEO Accession:GSM2399708 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 2500   SRP093723     ZMEL1_ATCACG_AHBENJADXX_L002_001.R1.fastq fastq 444225800.0 8884516.0 GSM2399708 r2 0:50 A:116866564;C:94744486;G:103253213;T:128645533;N:716004 50       116866564 94744486 103253213 128645533 716004 SRX2367694 SRS1813793 SRA497524 GEO White Lab, Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center 1 0.86139   0.32876   0.78259   0.62694   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified trueseq bulk unknown unknown   United States 2016-11-22 Larval Larval Cancer or Tumor Cancer or Tumor
41616 41616 SRR5099113 SRX2415891 SRS1853479 SRP094947 PRJNA357051 Development of zebrafish medulloblastoma model by TALENs induced somatic gene inactivation methods GSE92260 Transcriptome Analysis we developed the zebrafish cancer models by TALENs mediated somatic inactivation of tumor suppressor genes rb1 induced brain tumors in tp53 mutation background. Using RNA sequencing analysis in addition to histopathology and immunohistochemistry we demonstrated that the brain tumors induced by rb1 gene somatic inactivation have a molecular feature of MB like PNETs Overall design: QuantSeq three prime mRNA sequencing with whole brain tissue wild type WT zebrafish and tumors induced by rb1 TALENs injected zebrafish at xxx mpf   pubmed:28903419   FFPE 2 GSM2424730   source name:tumor 2 induced by rb1 TALENs|strain:p53M214K|tissue:tumor tissues 2 induced by rb1 TALENs|developmental stage:5 mpf FFPE 2 Illumina Casava1.8 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequenceusing fastx trimmer then mapped to danRer10 whole genome using Bowtie2 Read count extraction and nomalization were performed using edgeR. Genome build: danRer10 Supplementary files format and content: FFPE 1.txt and FFPE 2.txt report quantile normalized abundance measurements. Supplementary files format and content: WT.txt report quantile normalized abundance measurements. Column WT1 reports quantile normalized abundance measurements post quantile normalization had done between WT and FFPE 1. Column WT2 reports quantile normalized abundance measurements post quantile normalization had done between WT and FFPE 2. tumor 2 induced by rb1 TALENs   RNA was harvested using Trizol reagent Invitrogen. 500 ng of total RNA was used for the construction of sequencing libraries. RNA libraries were prepared for sequencing using LEXOGEN Quant Seq Library Prep Kit Cat#001.24 standard protocols.   strain:p53M214K|tissue:tumor tissues 2 induced by rb1 TALENs|developmental stage:5 mpf GSM2424730 GSM2424730: FFPE 2; Danio rerio; RNA Seq GSM2424730   1 RNA was harvested using Trizol reagent Invitrogen. 500 ng of total RNA was used for the construction of sequencing libraries. RNA libraries were prepared for sequencing using LEXOGEN Quant Seq Library Prep Kit Cat#001.24 standard protocols. GEO Accession:GSM2424730 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 500   SRP094947     FFPE-2_fastq.gz fastq 900420050.0 8915050.0 GSM2424730 r1 0:101 A:404381931;C:201118712;G:149335807;T:145550067;N:33533 101       404381931 201118712 149335807 145550067 33533 SRX2415891 SRS1853479 SRA502460 GEO Research Institute, National Cancer Center 1 0.03639   0.02825   0.9978   0.55688   101   B   usable mapping rate illumina nextseq 3prime cdna_unspecified lexogen bulk unknown unknown   Unknown 2016-12-12 Adult Adult Cancer or Tumor Cancer or Tumor
41617 41617 SRR5099112 SRX2415890 SRS1853478 SRP094947 PRJNA357051 Development of zebrafish medulloblastoma model by TALENs induced somatic gene inactivation methods GSE92260 Transcriptome Analysis we developed the zebrafish cancer models by TALENs mediated somatic inactivation of tumor suppressor genes rb1 induced brain tumors in tp53 mutation background. Using RNA sequencing analysis in addition to histopathology and immunohistochemistry we demonstrated that the brain tumors induced by rb1 gene somatic inactivation have a molecular feature of MB like PNETs Overall design: QuantSeq three prime mRNA sequencing with whole brain tissue wild type WT zebrafish and tumors induced by rb1 TALENs injected zebrafish at xxx mpf   pubmed:28903419   FFPE 1 GSM2424729   source name:tumor 1 induced by rb1 TALENs|strain:p53M214K|tissue:tumor tissues 1 induced by rb1 TALENs|developmental stage:5 mpf FFPE 1 Illumina Casava1.8 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequenceusing fastx trimmer then mapped to danRer10 whole genome using Bowtie2 Read count extraction and nomalization were performed using edgeR. Genome build: danRer10 Supplementary files format and content: FFPE 1.txt and FFPE 2.txt report quantile normalized abundance measurements. Supplementary files format and content: WT.txt report quantile normalized abundance measurements. Column WT1 reports quantile normalized abundance measurements post quantile normalization had done between WT and FFPE 1. Column WT2 reports quantile normalized abundance measurements post quantile normalization had done between WT and FFPE 2. tumor 1 induced by rb1 TALENs   RNA was harvested using Trizol reagent Invitrogen. 500 ng of total RNA was used for the construction of sequencing libraries. RNA libraries were prepared for sequencing using LEXOGEN Quant Seq Library Prep Kit Cat#001.24 standard protocols.   strain:p53M214K|tissue:tumor tissues 1 induced by rb1 TALENs|developmental stage:5 mpf GSM2424729 GSM2424729: FFPE 1; Danio rerio; RNA Seq GSM2424729   1 RNA was harvested using Trizol reagent Invitrogen. 500 ng of total RNA was used for the construction of sequencing libraries. RNA libraries were prepared for sequencing using LEXOGEN Quant Seq Library Prep Kit Cat#001.24 standard protocols. GEO Accession:GSM2424729 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 500   SRP094947     FFPE-1_fastq.gz fastq 985654556.0 9758956.0 GSM2424729 r1 0:101 A:642158389;C:109642019;G:103170689;T:130633868;N:49591 101       642158389 109642019 103170689 130633868 49591 SRX2415890 SRS1853478 SRA502460 GEO Research Institute, National Cancer Center 1 0.71847   0.59813   0.9376   0.57167   101   B   usable mapping rate illumina nextseq 3prime cdna_unspecified lexogen bulk unknown unknown   Unknown 2016-12-12 Adult Adult Cancer or Tumor Cancer or Tumor
41811 41811 SRR5196075 SRX2511746 SRS1935439 SRP097636 PRJNA362941 Transcriptomic analyses of Kras induced zebrafish liver cancer GSE93965 Transcriptome Analysis The krasV12 induced tumor progression was conducted on 100 transgenic fishes maintained in water containing 2µM mifepristone. Gross morphological and histological analyses were weekly performed on 15 randomly selected fishes to monitor tumor development. These analyses showed robust development of hepatocellular adenoma within 4 weeks of induction. Observation of tumor development and staging of tumorigenesis was conducted as described. For tumor regression the group of 15 fishes with HCC was transferred to mifepristone free water. Histological examination revealed tumor shrinkage showing extensive scarring at the peripheral and focal tumor regions. Notably complete tumor regression with scarred fibrosis of the former tumor tissue was observed post 4 weeks of mifepristone withdrawal. Overall design: Liver tumors from mifipristone induced transgenic fishes with hepatocellular adenoma and carcinoma livers of transgenic fishes post mifepristone withdrawal and normal livers from non induced and induced transgenic fishes were pooled separately and collected for RNA isolation and sequencing.   pubmed:31827597   CarcinomaM GSM2465779   source name:Hepatocellular carcinoma of transgenic fishes post mifeprist1 withdrawal|tissue:Hepatocellular carcinoma|genotype:Tgfabp10:LexPR LexA:EGFP; cryB:mCherry NLS Cre; fabp10:loxP mCherry loxP EGFP krasV12 line CarcinomaM The SOLiD generated RNA Seq reads was in 27 bp length and an initial filtering process was taken to remove any non desirable contamination sequences. The reads were mapped to the zebrafish NCBI RefSeq Reference Sequence mRNA database with a criterion of maximum 2 nucleotide mismatches. The expression levels of mapped transcripts were normalized into transcript per whole amount of mapped transcript. Genome build: danRer7 Supplementary files format and content: tab delimited text files include TPM values for each Sample Hepatocellular carcinoma of transgenic fishes post mifepristone withdrawal One mpf transgenic fish was treated at 2uM mifepriston to induce liver tumorigenesis. For tumor regression the group of 15 fishes with HCC was transferred to mifepristone free water. mRNA was purified using Dynabeads OligodT EcoP Invitrogen Resultant cDNA was digested by NlaIII and EcoP15I to result in a 27 nucleotides cDNA tag between the two sequencing adapters. 3′ RNA SAGE serial analysis of gene expression sequencing was performed on ABI SOLiD platform by Mission Biotech Taiwan according to manufacturer’s protocol and 10–23 million reads were generated from each sample   tissue:Hepatocellular carcinoma|genotype:Tgfabp10:LexPR LexA:EGFP; cryB:mCherry NLS Cre; fabp10:loxP mCherry loxP EGFP krasV12 line GSM2465779 GSM2465779: CarcinomaM; Danio rerio; RNA Seq GSM2465779   1 mRNA was purified using Dynabeads OligodT EcoP Invitrogen Resultant cDNA was digested by NlaIII and EcoP15I to result in a 27 nucleotides cDNA tag between the two sequencing adapters. 3′ RNA SAGE serial analysis of gene expression sequencing was performed on ABI SOLiD platform by Mission Biotech Taiwan according to manufacturer’s protocol and 10–23 million reads were generated from each sample GEO Accession:GSM2465779 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ABI_SOLID AB SOLiD System 3.0   SRP097636     solid_SAGE_6T2_F3.csfasta.gz solid_SAGE_6T2_F3_QV.qual.gz SOLiD_native SOLiD_native 818910190.0 23397434.0 GSM2465779 r1 0:35 0:347259734;1:164743259;2:162029194;3:130508344;.:14369659 35                 SRX2511746 SRS1935439 SRA530985 GEO The Biomedical Center 1 0.03756   0.00615   0.99928   0.91338   35   B   usable mapping rate legacy early unknown poly_a unknown bulk unknown unknown   Unknown 2017-01-23 Undetermined Adult Cancer or Tumor Cancer or Tumor
41812 41812 SRR5196074 SRX2511745 SRS1935438 SRP097636 PRJNA362941 Transcriptomic analyses of Kras induced zebrafish liver cancer GSE93965 Transcriptome Analysis The krasV12 induced tumor progression was conducted on 100 transgenic fishes maintained in water containing 2µM mifepristone. Gross morphological and histological analyses were weekly performed on 15 randomly selected fishes to monitor tumor development. These analyses showed robust development of hepatocellular adenoma within 4 weeks of induction. Observation of tumor development and staging of tumorigenesis was conducted as described. For tumor regression the group of 15 fishes with HCC was transferred to mifepristone free water. Histological examination revealed tumor shrinkage showing extensive scarring at the peripheral and focal tumor regions. Notably complete tumor regression with scarred fibrosis of the former tumor tissue was observed post 4 weeks of mifepristone withdrawal. Overall design: Liver tumors from mifipristone induced transgenic fishes with hepatocellular adenoma and carcinoma livers of transgenic fishes post mifepristone withdrawal and normal livers from non induced and induced transgenic fishes were pooled separately and collected for RNA isolation and sequencing.   pubmed:31827597   Carcinoma GSM2465778   source name:Hepatocellular carcinoma of transgenic fishes|tissue:Hepatocellular carcinoma|genotype:Tgfabp10:LexPR LexA:EGFP; cryB:mCherry NLS Cre; fabp10:loxP mCherry loxP EGFP krasV12 line Carcinoma The SOLiD generated RNA Seq reads was in 27 bp length and an initial filtering process was taken to remove any non desirable contamination sequences. The reads were mapped to the zebrafish NCBI RefSeq Reference Sequence mRNA database with a criterion of maximum 2 nucleotide mismatches. The expression levels of mapped transcripts were normalized into transcript per whole amount of mapped transcript. Genome build: danRer7 Supplementary files format and content: tab delimited text files include TPM values for each Sample Hepatocellular carcinoma of transgenic fishes One mpf transgenic fish was treated at 2uM mifepriston to induce liver tumorigenesis. For tumor regression the group of 15 fishes with HCC was transferred to mifepristone free water. mRNA was purified using Dynabeads OligodT EcoP Invitrogen Resultant cDNA was digested by NlaIII and EcoP15I to result in a 27 nucleotides cDNA tag between the two sequencing adapters. 3′ RNA SAGE serial analysis of gene expression sequencing was performed on ABI SOLiD platform by Mission Biotech Taiwan according to manufacturer’s protocol and 10–23 million reads were generated from each sample   tissue:Hepatocellular carcinoma|genotype:Tgfabp10:LexPR LexA:EGFP; cryB:mCherry NLS Cre; fabp10:loxP mCherry loxP EGFP krasV12 line GSM2465778 GSM2465778: Carcinoma; Danio rerio; RNA Seq GSM2465778   1 mRNA was purified using Dynabeads OligodT EcoP Invitrogen Resultant cDNA was digested by NlaIII and EcoP15I to result in a 27 nucleotides cDNA tag between the two sequencing adapters. 3′ RNA SAGE serial analysis of gene expression sequencing was performed on ABI SOLiD platform by Mission Biotech Taiwan according to manufacturer’s protocol and 10–23 million reads were generated from each sample GEO Accession:GSM2465778 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ABI_SOLID AB SOLiD System 3.0   SRP097636     solid_SAGE_6T1_F3.csfasta.gz solid_SAGE_6T1_F3_QV.qual.gz SOLiD_native SOLiD_native 761241005.0 21749743.0 GSM2465778 r1 0:35 0:306840116;1:164725874;2:160786359;3:126370697;.:2517959 35                 SRX2511745 SRS1935438 SRA530985 GEO The Biomedical Center 1 0.0543   0.00668   0.9988   0.95092   35   B   usable mapping rate legacy early unknown poly_a unknown bulk unknown unknown   Unknown 2017-01-23 Undetermined Adult 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
50848 50848 SRR8312803 SRX5126180 SRS4139302 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1314 GSM3509262   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1314 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509262 GSM3509262: nonSP 1314; Danio rerio; RNA Seq GSM3509262   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509262 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         1102240750.0 22044815.0 GSM3509262 r1 0:50 1:0 A:238366338;C:290902481;G:270336209;T:302466123;N:169599 50 0     238366338 290902481 270336209 302466123 169599 SRX5126180 SRS4139302 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.95733   0.05326   0.82195   0.45391   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50849 50849 SRR8312804 SRX5126180 SRS4139302 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1314 GSM3509262   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1314 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509262 GSM3509262: nonSP 1314; Danio rerio; RNA Seq GSM3509262   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509262 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         2100323600.0 42006472.0 GSM3509262 r2 0:50 1:0 A:454665602;C:553824333;G:514968464;T:576182722;N:682479 50 0     454665602 553824333 514968464 576182722 682479 SRX5126180 SRS4139302 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.95581   0.05304   0.82246   0.44598   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50850 50850 SRR8312801 SRX5126179 SRS4139301 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1314 GSM3509261   source name:ALL tumor|strain:CG2|tissue:ALL SP 1314 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509261 GSM3509261: SP 1314; Danio rerio; RNA Seq GSM3509261   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509261 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         1795016300.0 35900326.0 GSM3509261 r1 0:50 1:0 A:414364764;C:453952517;G:425127792;T:501295946;N:275281 50 0     414364764 453952517 425127792 501295946 275281 SRX5126179 SRS4139301 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.94054   0.1034   0.77199   0.50665   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50851 50851 SRR8312802 SRX5126179 SRS4139301 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1314 GSM3509261   source name:ALL tumor|strain:CG2|tissue:ALL SP 1314 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509261 GSM3509261: SP 1314; Danio rerio; RNA Seq GSM3509261   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509261 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         1643807200.0 32876144.0 GSM3509261 r2 0:50 1:0 A:379875320;C:415331594;G:389155351;T:458912143;N:532792 50 0     379875320 415331594 389155351 458912143 532792 SRX5126179 SRS4139301 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.93812   0.1016   0.77281   0.50853   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50852 50852 SRR8312799 SRX5126178 SRS4139300 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1279 GSM3509260   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1279 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509260 GSM3509260: nonSP 1279; Danio rerio; RNA Seq GSM3509260   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509260 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         971515350.0 19430307.0 GSM3509260 r1 0:50 1:0 A:209882045;C:255304153;G:238689373;T:267489989;N:149790 50 0     209882045 255304153 238689373 267489989 149790 SRX5126178 SRS4139300 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.96223   0.08865   0.85437   0.45664   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50853 50853 SRR8312800 SRX5126178 SRS4139300 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1279 GSM3509260   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1279 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509260 GSM3509260: nonSP 1279; Danio rerio; RNA Seq GSM3509260   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509260 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         859048800.0 17180976.0 GSM3509260 r2 0:50 1:0 A:185797914;C:225529235;G:211061558;T:236378727;N:281366 50 0     185797914 225529235 211061558 236378727 281366 SRX5126178 SRS4139300 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.96055   0.08804   0.85283   0.48896   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50854 50854 SRR8312797 SRX5126177 SRS4139299 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1279 GSM3509259   source name:ALL tumor|strain:CG2|tissue:ALL SP 1279 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509259 GSM3509259: SP 1279; Danio rerio; RNA Seq GSM3509259   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509259 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         843819050.0 16876381.0 GSM3509259 r1 0:50 1:0 A:199287616;C:210295815;G:195583208;T:238522867;N:129544 50 0     199287616 210295815 195583208 238522867 129544 SRX5126177 SRS4139299 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.9391   0.1451   0.79683   0.50281   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50855 50855 SRR8312798 SRX5126177 SRS4139299 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1279 GSM3509259   source name:ALL tumor|strain:CG2|tissue:ALL SP 1279 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509259 GSM3509259: SP 1279; Danio rerio; RNA Seq GSM3509259   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509259 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         2285635100.0 45712702.0 GSM3509259 r2 0:50 1:0 A:540527368;C:568996224;G:529423615;T:645948448;N:739445 50 0     540527368 568996224 529423615 645948448 739445 SRX5126177 SRS4139299 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.93725   0.14453   0.79746   0.4961   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50856 50856 SRR8312795 SRX5126176 SRS4139298 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1404 GSM3509258   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1404 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509258 GSM3509258: nonSP 1404; Danio rerio; RNA Seq GSM3509258   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509258 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         2069543600.0 41390872.0 GSM3509258 r1 0:50 1:0 A:459382162;C:532071054;G:508544948;T:569228380;N:317056 50 0     459382162 532071054 508544948 569228380 317056 SRX5126176 SRS4139298 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.96095   0.06905   0.83412   0.4818   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50857 50857 SRR8312796 SRX5126176 SRS4139298 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   nonSP 1404 GSM3509258   source name:ALL tumor|strain:CG2|tissue:ALL nonSP 1404 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509258 GSM3509258: nonSP 1404; Danio rerio; RNA Seq GSM3509258   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509258 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         1547447200.0 30948944.0 GSM3509258 r2 0:50 1:0 A:343821341;C:397523901;G:380174292;T:425426296;N:501370 50 0     343821341 397523901 380174292 425426296 501370 SRX5126176 SRS4139298 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.95838   0.06884   0.83414   0.48727   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50858 50858 SRR8312793 SRX5126175 SRS4139297 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1404 GSM3509257   source name:ALL tumor|strain:CG2|tissue:ALL SP 1404 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509257 GSM3509257: SP 1404; Danio rerio; RNA Seq GSM3509257   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509257 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         2020346850.0 40406937.0 GSM3509257 r1 0:50 1:0 A:476259938;C:502400578;G:476364320;T:565010528;N:311486 50 0     476259938 502400578 476364320 565010528 311486 SRX5126175 SRS4139297 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.94163   0.11567   0.79287   0.52008   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
50859 50859 SRR8312794 SRX5126175 SRS4139297 SRP173302 PRJNA509471 The side population enriches for leukemia propagating cell activity and Wnt pathway expression in zebrafish acute lymphoblastic leukemia. GSE123665 Transcriptome Analysis Cancer stem cells have been strongly linked to resistance and relapse in many malignancies. However purifying them from within the bulk tumor has been challenging so their precise genetic and functional characteristics are not well defined. The side population assay exploits the ability of some cells to efflux Hoechst dye via ABC transporters. Stem cells have increased expression of these transporters and this assay has been shown to enrich for stem cells in various tissues and cancers. This study identifies the side population within a zebrafish model of acute lymphoblastic leukemia and correlates the frequency of side population cells with the frequency of leukemia stem cells more precisely referred to as leukemia propagating cells within our transplantation model. In addition the side population within the leukemia evolves with serial transplantation increasing in tandem with leukemia propagating cell frequency over subsequent generations. Sorted side population cells from these tumors are enriched for leukemia propagating cells and have enhanced engraftment compared to sorted non side population cells when transplanted into syngeneic recipients. RNA sequencing analysis of sorted side population cells compared to non side population cells identified a shared expression profile within the side population and pathway analysis yielded Wnt signaling as the most overrepresented. Gene set enrichment analysis showed that stem cell differentiation and canonical Wnt signaling were significantly upregulated in the side population. Overall these results demonstrate that the side population in zebrafish acute lymphoblastic leukemia significantly enriches for leukemia propagating cells and identifies the Wnt pathway as a likely genetic driver of leukemia stem cell fate. Overall design: mRNA expression comparison between sorted side population and non side population in 3 zebrafish ALL tumors   pubmed:30630989   SP 1404 GSM3509257   source name:ALL tumor|strain:CG2|tissue:ALL SP 1404 Illumina Casava1.7 software used for basecalling. All RNA seq reads were used to align to the genome assembly GRCz10 using STAR v2.5.1b with default configurations. Transcripts were assembled from the aligned reads using Cufflinks v2.2.1 with the default configurations to generate FPKM Fragments Per Kilobase Million tables. Using 4 as the fold change cutoff DEGs Differentially expressed genes were detected using both Tuxedo suite FPKM based method and featureCounts DESeq v1.30.0 edgeR v3.20.7 read count based method with default configurations. Genes detected by at least more than one method were collected to create a high confidence DEG lists. Genome build: GRCz10 Supplementary files format and content: Count tables were generated using featureCount v1.28.1 based on Ensembl annotation GRCz10. ALL tumor None Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols None strain:CG2|tissue:ALL GSM3509257 GSM3509257: SP 1404; Danio rerio; RNA Seq GSM3509257   1 Tumors were removed sorted by FACS and RNA was harvested using Trizol reagent. RNA libraries were prepared for sequencing using standard Illumina protocols GEO Accession:GSM3509257 RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA Illumina HiSeq 4000   SRP173302         1560387300.0 31207746.0 GSM3509257 r2 0:50 1:0 A:368229806;C:387650010;G:367757630;T:436243680;N:506174 50 0     368229806 387650010 367757630 436243680 506174 SRX5126175 SRS4139297 SRA822847 GEO Bioinformatics Core, Biological Sciences Division, The University of Chicago 1 0.93995   0.11774   0.79444   0.49697   50   B   usable mapping rate illumina hiseq_era unknown cdna_unspecified unknown bulk unknown unknown   United States 2018-12-11 Undetermined Undetermined 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

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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");;