metadata: run_metadata: 31 rows where experiment.library_layout = "PAIRED", experiment.platform = "BGISEQ" and tissue

31 rows where experiment.library_layout = "PAIRED", experiment.platform = "BGISEQ" and tissue_curation = "Cancer or Tumor"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	study.attributes	study.PMIDs	sample.title	sample.alias	sample.attributes	GEOsample.title	GEOsample.dataprocessing	GEOsample.source	GEOsample.treatmentprotocol	GEOsample.extractprotocol	GEOsample.growthprotocol	GEOsample.characteristics	GEOsample.accession	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_construction_protocol	experiment.attributes	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.n_mates	seqdetective.mapping_rate.mate1	seqdetective.mapping_rate.mate2	seqdetective.nofeature_rate.mate1	seqdetective.nofeature_rate.mate2	seqdetective.sparsity.mate1	seqdetective.sparsity.mate2	seqdetective.pos_strand_rate.mate1	seqdetective.pos_strand_rate.mate2	seqdetective.readlen.mate1	seqdetective.readlen.mate2	seqdetective.judgement.mate1	seqdetective.judgement.mate2	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
66210	66210	SRR16102702	SRX12388690	SRS10358692	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day3 rep3 RNA Seq	GSM5602251	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day3 rep3 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602251	GSM5602251: Tumor cells JQ1 day3 rep3 RNA Seq; Danio rerio; RNA Seq	GSM5602251		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602251	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_J3_1.fq.gz D3_J3_2.fq.gz	fastq fastq	4552030000.0	45520300.0	GSM5602251 r1	0:100 1:100	A:1214627731;C:1045617960;G:1070259567;T:1221524742;N:0	100	100	1214627731	1045617960	1070259567	1221524742	SRX12388690	SRS10358692	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.93576		0.23142		0.74144		0.48177		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66211	66211	SRR16102701	SRX12388689	SRS10358691	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day3 rep2 RNA Seq	GSM5602250	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day3 rep2 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602250	GSM5602250: Tumor cells JQ1 day3 rep2 RNA Seq; Danio rerio; RNA Seq	GSM5602250		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602250	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_J2_1.fq.gz D3_J2_2.fq.gz	fastq fastq	4475915200.0	44759152.0	GSM5602250 r1	0:100 1:100	A:1189464447;C:1030660361;G:1055524478;T:1200265914;N:0	100	100	1189464447	1030660361	1055524478	1200265914	SRX12388689	SRS10358691	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94062		0.18735		0.69759		0.49542		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66212	66212	SRR16102700	SRX12388688	SRS10358690	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day3 rep1 RNA Seq	GSM5602249	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day3 rep1 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602249	GSM5602249: Tumor cells JQ1 day3 rep1 RNA Seq; Danio rerio; RNA Seq	GSM5602249		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602249	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_J1_1.fq.gz D3_J1_2.fq.gz	fastq fastq	4442146800.0	44421468.0	GSM5602249 r1	0:100 1:100	A:1179373951;C:1024313469;G:1050720604;T:1187738776;N:0	100	100	1179373951	1024313469	1050720604	1187738776	SRX12388688	SRS10358690	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94195		0.23006		0.72894		0.4972		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66213	66213	SRR16102699	SRX12388687	SRS10358689	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day3 rep3 RNA Seq	GSM5602248	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day3 rep3 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602248	GSM5602248: Tumor cells DMSO day3 rep3 RNA Seq; Danio rerio; RNA Seq	GSM5602248		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602248	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_D3_1.fq.gz D3_D3_2.fq.gz	fastq fastq	4446401600.0	44464016.0	GSM5602248 r1	0:100 1:100	A:1202900253;C:1006105416;G:1022157182;T:1215238749;N:0	100	100	1202900253	1006105416	1022157182	1215238749	SRX12388687	SRS10358689	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.95301		0.35614		0.79961		0.50405		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66214	66214	SRR16102698	SRX12388686	SRS10358687	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day3 rep2 RNA Seq	GSM5602247	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day3 rep2 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602247	GSM5602247: Tumor cells DMSO day3 rep2 RNA Seq; Danio rerio; RNA Seq	GSM5602247		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602247	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_D2_1.fq.gz D3_D2_2.fq.gz	fastq fastq	4459355600.0	44593556.0	GSM5602247 r1	0:100 1:100	A:1202802143;C:1015451294;G:1025320457;T:1215781706;N:0	100	100	1202802143	1015451294	1025320457	1215781706	SRX12388686	SRS10358687	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.9443		0.32993		0.77786		0.50186		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66215	66215	SRR16102697	SRX12388685	SRS10358686	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day3 rep1 RNA Seq	GSM5602246	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day3 rep1 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602246	GSM5602246: Tumor cells DMSO day3 rep1 RNA Seq; Danio rerio; RNA Seq	GSM5602246		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602246	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D3_D1_1.fq.gz D3_D1_2.fq.gz	fastq fastq	4486671200.0	44866712.0	GSM5602246 r1	0:100 1:100	A:1182551057;C:1045032741;G:1067880067;T:1191207335;N:0	100	100	1182551057	1045032741	1067880067	1191207335	SRX12388685	SRS10358686	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94059		0.21995		0.76658		0.47389		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66216	66216	SRR16102696	SRX12388684	SRS10358685	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day1 rep3 RNA Seq	GSM5602245	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day1 rep3 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602245	GSM5602245: Tumor cells JQ1 day1 rep3 RNA Seq; Danio rerio; RNA Seq	GSM5602245		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602245	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_J3_1.fq.gz D1_J3_2.fq.gz	fastq fastq	4550470000.0	45504700.0	GSM5602245 r1	0:100 1:100	A:1213052369;C:1047508174;G:1069309019;T:1220600438;N:0	100	100	1213052369	1047508174	1069309019	1220600438	SRX12388684	SRS10358685	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94051		0.24901		0.74899		0.50515		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66217	66217	SRR16102695	SRX12388683	SRS10358684	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day1 rep2 RNA Seq	GSM5602244	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day1 rep2 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602244	GSM5602244: Tumor cells JQ1 day1 rep2 RNA Seq; Danio rerio; RNA Seq	GSM5602244		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602244	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_J2_1.fq.gz D1_J2_2.fq.gz	fastq fastq	4490144800.0	44901448.0	GSM5602244 r1	0:100 1:100	A:1197596235;C:1031109315;G:1057301946;T:1204137304;N:0	100	100	1197596235	1031109315	1057301946	1204137304	SRX12388683	SRS10358684	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94477		0.24522		0.74042		0.51025		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66218	66218	SRR16102694	SRX12388682	SRS10358688	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells JQ1 day1 rep1 RNA Seq	GSM5602243	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	Tumor cells JQ1 day1 rep1 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:treatment\|treatment:JQ1	GSM5602243	GSM5602243: Tumor cells JQ1 day1 rep1 RNA Seq; Danio rerio; RNA Seq	GSM5602243		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602243	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_J1_1.fq.gz D1_J1_2.fq.gz	fastq fastq	4434887800.0	44348878.0	GSM5602243 r1	0:100 1:100	A:1178050199;C:1024865996;G:1046777721;T:1185193884;N:0	100	100	1178050199	1024865996	1046777721	1185193884	SRX12388682	SRS10358688	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94501		0.2305		0.76432		0.49472		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66219	66219	SRR16102693	SRX12388681	SRS10358683	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day1 rep3 RNA Seq	GSM5602242	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day1 rep3 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602242	GSM5602242: Tumor cells DMSO day1 rep3 RNA Seq; Danio rerio; RNA Seq	GSM5602242		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602242	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_D3_1.fq.gz D1_D3_2.fq.gz	fastq fastq	4497882800.0	44978828.0	GSM5602242 r1	0:100 1:100	A:1193693228;C:1038160916;G:1064460652;T:1201568004;N:0	100	100	1193693228	1038160916	1064460652	1201568004	SRX12388681	SRS10358683	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.93714		0.19697		0.74554		0.50928		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66220	66220	SRR16102692	SRX12388680	SRS10358682	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day1 rep2 RNA Seq	GSM5602241	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day1 rep2 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602241	GSM5602241: Tumor cells DMSO day1 rep2 RNA Seq; Danio rerio; RNA Seq	GSM5602241		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602241	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_D2_1.fq.gz D1_D2_2.fq.gz	fastq fastq	4464096200.0	44640962.0	GSM5602241 r1	0:100 1:100	A:1185692334;C:1031585570;G:1050205768;T:1196612528;N:0	100	100	1185692334	1031585570	1050205768	1196612528	SRX12388680	SRS10358682	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94785		0.24425		0.78165		0.4975		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
66221	66221	SRR16102691	SRX12388679	SRS10358681	SRP339154	PRJNA767083	RNA seq analysis for IRF4 driven zebrafish tumors post JQ1 treatment	GSE184946	Transcriptome Analysis	RNA seq analysis was performed using tumor cells driven by IRF4 to analyze gene expression changes post JQ1 treatment Overall design: The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1 or control DMSO for 1 or 3 days. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	parent bioproject:PRJNA701471	pubmed:35504924	Tumor cells DMSO day1 rep1 RNA Seq	GSM5602240	tissue:Zebrafish tumor cells\|cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	Tumor cells DMSO day1 rep1 RNA Seq	RNA seq datasets of DMSO treated control samples and JQ1 treated samples were aligned to the GRCz11 zebrafish genome Ensembl annotation with ERCC spike in information using STAR 2.5.2a with the parameter outFilterMultimapNmax set to 1. featureCount was used for the mapped reads in .bam files to generate count tables based on the Ensembl gene annotation and ERCC annotation. Bioconductor package DESeq2 v1.12.4 was used to analyze differential gene expression using 3 DMSO vs 3 JQ1 treated samples. Genome build: danRer11 Supplementary files format and content: featureCount read count for all sample DESeq2 files for differentially expressed genes	Zebrafish tumor cells	JQ1 was dissolved in DMSO. Animals were treated with JQ1 at 4microM or the same amount of DMSO in individual tanks for 1 or 3 days. Experiments were done using 3 independent animals.	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	The human IRF4 gene and mCherry fluorescent marker gene were transduced under the zebrafish lck promoter in zebrafish. post the development of lymphoma phenotype animals were treated with JQ1. Tumor cells were harvested and sorted by flow cytometry based on mCherry fluorescence expression. Total RNAs were harvested from each sample and then applied for RNA seq analysis.	cell type:Zebrafish tumor cells\|condition:control\|treatment:DMSO	GSM5602240	GSM5602240: Tumor cells DMSO day1 rep1 RNA Seq; Danio rerio; RNA Seq	GSM5602240		1	Total RNA was harvested using the miRNeasy Mini Kit Qiagen. ERCC spike in was added based on the total cell number. Strand specific library construction and sequencing of paired end 100 bp long reads by the BGISeq500 were performed at the BGI Biotech Solutions Hong Kong Co Ltd Hong Kong.	GEO Accession:GSM5602240	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	BGISEQ	BGISEQ-500	SRP339154	D1_D1_1.fq.gz D1_D1_2.fq.gz	fastq fastq	4466502200.0	44665022.0	GSM5602240 r1	0:100 1:100	A:1191785539;C:1024344626;G:1050598581;T:1199773454;N:0	100	100	1191785539	1024344626	1050598581	1199773454	SRX12388679	SRS10358681	SRA1302013	GEO	Takaomi Sanda Lab, Cancer Science Institute, National University of Singapore	1	0.94073		0.24308		0.77094		0.48493		100		B		usable mapping rate	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Singapore	2021-09-28	Undetermined	Undetermined	Cancer or Tumor	Cancer or Tumor
74560	74560	SRR23829118	SRX19650818	SRS17019470	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/10	7B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep4\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	7B	7B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	7B_1.fq.gz 7B_2.fq.gz	fastq fastq	10796340200.0	53981701.0	7B 1.fq.gz	0:100 1:100	A:2946489343;C:2411825502;G:2477056291;T:2960969064;N:0	100	100	2946489343	2411825502	2477056291	2960969064	SRX19650818	SRS17019470	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91639	0.92098	0.13624	0.1358	0.7443	0.74367	0.52593	0.52158	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74561	74561	SRR23829119	SRX19650817	SRS17019469	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/12	8B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep5\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	8B	8B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	8B_1.fq.gz 8B_2.fq.gz	fastq fastq	10560562800.0	52802814.0	8B 1.fq.gz	0:100 1:100	A:2867789187;C:2366678430;G:2438457525;T:2887637658;N:0	100	100	2867789187	2366678430	2438457525	2887637658	SRX19650817	SRS17019469	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.90976	0.91391	0.15248	0.15201	0.73499	0.73379	0.51572	0.51882	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74562	74562	SRR23829120	SRX19650816	SRS17019468	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2806/1	9B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:28.06.2021\|genotype:tert / rep4\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	9B	9B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	9B_1.fq.gz 9B_2.fq.gz	fastq fastq	10805598600.0	54027993.0	9B 1.fq.gz	0:100 1:100	A:2899169569;C:2457980147;G:2528851393;T:2919597491;N:0	100	100	2899169569	2457980147	2528851393	2919597491	SRX19650816	SRS17019468	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92637	0.93052	0.12486	0.12507	0.73352	0.73188	0.51498	0.52101	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74563	74563	SRR23829121	SRX19650815	SRS17019467	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2806/2	10B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:28.06.2021\|genotype:tert+/+ rep1\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	10B	10B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	10B_1.fq.gz 10B_2.fq.gz	fastq fastq	10811556000.0	54057780.0	10B 1.fq.gz	0:100 1:100	A:2898576858;C:2460872365;G:2527128196;T:2924978581;N:0	100	100	2898576858	2460872365	2527128196	2924978581	SRX19650815	SRS17019467	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92176	0.92836	0.12295	0.12256	0.72604	0.72458	0.51306	0.51966	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74564	74564	SRR23829122	SRX19650814	SRS17019466	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/9	6B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep3\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	6B	6B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	6B_1.fq.gz 6B_2.fq.gz	fastq fastq	10809952000.0	54049760.0	6B 1.fq.gz	0:100 1:100	A:2931041183;C:2429723251;G:2502283305;T:2946904261;N:0	100	100	2931041183	2429723251	2502283305	2946904261	SRX19650814	SRS17019466	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92179	0.92775	0.13661	0.1365	0.74679	0.74556	0.52477	0.52471	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74565	74565	SRR23829123	SRX19650813	SRS17019465	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/8	5B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep2\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	5B	5B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	5B_1.fq.gz 5B_2.fq.gz	fastq fastq	10604822000.0	53024110.0	5B 1.fq.gz	0:100 1:100	A:2847359136;C:2411906169;G:2481911629;T:2863645066;N:0	100	100	2847359136	2411906169	2481911629	2863645066	SRX19650813	SRS17019465	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92231	0.92771	0.13302	0.13258	0.74052	0.73843	0.51718	0.51163	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74566	74566	SRR23829124	SRX19650812	SRS17019464	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/7	4B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep1\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	4B	4B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	4B_1.fq.gz 4B_2.fq.gz	fastq fastq	10792140600.0	53960703.0	4B 1.fq.gz	0:100 1:100	A:2882693797;C:2464129073;G:2535344124;T:2909973606;N:0	100	100	2882693797	2464129073	2535344124	2909973606	SRX19650812	SRS17019464	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91884	0.92345	0.12967	0.12884	0.74117	0.74103	0.50792	0.51065	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74567	74567	SRR23829125	SRX19650811	SRS17019463	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/4	3B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert / rep3\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	3B	3B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	3B_1.fq.gz 3B_2.fq.gz	fastq fastq	10817072400.0	54085362.0	3B 1.fq.gz	0:100 1:100	A:2980754877;C:2390812269;G:2448674730;T:2996830524;N:0	100	100	2980754877	2390812269	2448674730	2996830524	SRX19650811	SRS17019463	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91015	0.9166	0.15854	0.15694	0.73724	0.73442	0.5243	0.52496	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74568	74568	SRR23829126	SRX19650810	SRS17019462	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2104/14	19B	strain:AB\|age:10 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:21.04.2021\|genotype:tert / rep3\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 10 month male tumor	19B	19B	RNA Seq of Danio rerio : 10 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	19B_1.fq.gz 19B_2.fq.gz	fastq fastq	12603676000.0	63018380.0	19B 1.fq.gz	0:100 1:100	A:3414935292;C:2859787251;G:2916851430;T:3412102027;N:0	100	100	3414935292	2859787251	2916851430	3412102027	SRX19650810	SRS17019462	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92494	0.92995	0.12064	0.12054	0.73807	0.73649	0.52554	0.52564	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74569	74569	SRR23829127	SRX19650809	SRS17019461	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2104/9	18B	strain:AB\|age:10 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:21.04.2021\|genotype:tert / rep2\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 10 month male tumor	18B	18B	RNA Seq of Danio rerio : 10 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	18B_1.fq.gz 18B_2.fq.gz	fastq fastq	12562625800.0	62813129.0	18B 1.fq.gz	0:100 1:100	A:3435125429;C:2818006678;G:2880078673;T:3429415020;N:0	100	100	3435125429	2818006678	2880078673	3429415020	SRX19650809	SRS17019461	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92476	0.92851	0.12505	0.12384	0.74961	0.74882	0.52843	0.52817	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74570	74570	SRR23829128	SRX19650808	SRS17019460	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2104/1	17B	strain:AB\|age:10 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:21.04.2021\|genotype:tert+/+ rep5\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 10 month male tumor	17B	17B	RNA Seq of Danio rerio : 10 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	17B_1.fq.gz 17B_2.fq.gz	fastq fastq	8787148400.0	43935742.0	17B 1.fq.gz	0:100 1:100	A:2617726378;C:1773416208;G:1829194025;T:2566811789;N:0	100	100	2617726378	1773416208	1829194025	2566811789	SRX19650808	SRS17019460	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.84629	0.85164	0.49471	0.49585	0.79545	0.79275	0.64785	0.57659	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74571	74571	SRR23829129	SRX19650807	SRS17019459	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2806/3	16B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:28.06.2021\|genotype:tert+/+ rep4\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	16B	16B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	16B_1.fq.gz 16B_2.fq.gz	fastq fastq	12372317000.0	61861585.0	16B 1.fq.gz	0:100 1:100	A:3325923130;C:2824746317;G:2889873754;T:3331773799;N:0	100	100	3325923130	2824746317	2889873754	3331773799	SRX19650807	SRS17019459	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92023	0.92579	0.13379	0.13406	0.75974	0.75954	0.51721	0.53155	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74572	74572	SRR23829130	SRX19650806	SRS17019458	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2506/2	15B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:25.06.2021\|genotype:tert+/+ rep3\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	15B	15B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	15B_1.fq.gz 15B_2.fq.gz	fastq fastq	12111580000.0	60557900.0	15B 1.fq.gz	0:100 1:100	A:3253473957;C:2781714853;G:2829572138;T:3246819052;N:0	100	100	3253473957	2781714853	2829572138	3246819052	SRX19650806	SRS17019458	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92909	0.9333	0.12994	0.13008	0.76997	0.76921	0.53473	0.52603	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74573	74573	SRR23829131	SRX19650805	SRS17019457	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2506/1	14B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:25.06.2021\|genotype:tert / rep1\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	14B	14B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	14B_1.fq.gz 14B_2.fq.gz	fastq fastq	12314492000.0	61572460.0	14B 1.fq.gz	0:100 1:100	A:3364570176;C:2760126284;G:2813170851;T:3376624689;N:0	100	100	3364570176	2760126284	2813170851	3376624689	SRX19650805	SRS17019457	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.92824	0.93249	0.16314	0.16227	0.74217	0.74142	0.54103	0.54082	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74574	74574	SRR23829132	SRX19650804	SRS17019456	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/11	13B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert+/+ rep6\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	13B	13B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	13B_1.fq.gz 13B_2.fq.gz	fastq fastq	12281192200.0	61405961.0	13B 1.fq.gz	0:100 1:100	A:3369650885;C:2745871807;G:2821246280;T:3344423228;N:0	100	100	3369650885	2745871807	2821246280	3344423228	SRX19650804	SRS17019456	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.93143	0.93303	0.1814	0.18252	0.76207	0.76169	0.55108	0.54553	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74575	74575	SRR23829133	SRX19650803	SRS17019455	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/2	12B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert / rep4\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	12B	12B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	12B_1.fq.gz 12B_2.fq.gz	fastq fastq	12163842800.0	60819214.0	12B 1.fq.gz	0:100 1:100	A:3431206764;C:2629189354;G:2672190281;T:3431256401;N:0	100	100	3431206764	2629189354	2672190281	3431256401	SRX19650803	SRS17019455	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91204	0.91933	0.22594	0.22625	0.73777	0.73586	0.5046	0.47081	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74576	74576	SRR23829134	SRX19650802	SRS17019454	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			2806/4	11B	strain:AB\|age:12 month\|sex:male\|tissue:Tumor\|birth date:24.06.2020\|birth location:PEMAV IRCAN France\|death date:28.06.2021\|genotype:tert+/+ rep2\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 12 month male tumor	11B	11B	RNA Seq of Danio rerio : 12 month male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	11B_1.fq.gz 11B_2.fq.gz	fastq fastq	10583058000.0	52915290.0	11B 1.fq.gz	0:100 1:100	A:2970647072;C:2293859072;G:2357521919;T:2961029937;N:0	100	100	2970647072	2293859072	2357521919	2961029937	SRX19650802	SRS17019454	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.90787	0.91228	0.1916	0.19016	0.72271	0.72092	0.52084	0.52228	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74577	74577	SRR23829135	SRX19650801	SRS17019453	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/3	2B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert / rep2\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	2B	2B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	2B_1.fq.gz 2B_2.fq.gz	fastq fastq	10776715000.0	53883575.0	2B 1.fq.gz	0:100 1:100	A:2948670507;C:2400698003;G:2461964006;T:2965382484;N:0	100	100	2948670507	2400698003	2461964006	2965382484	SRX19650801	SRS17019453	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91594	0.91925	0.17372	0.17392	0.73708	0.73742	0.52748	0.53599	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor
74578	74578	SRR23829136	SRX19650800	SRS17019452	SRP426991	PRJNA944150	Absence of telomerase restricts melanoma development.	PRJNA944150	Other	Most cancers reactivate telomerase to maintain telomere length to acquire immortality. The importance of this process is well illustrated by the fact that telomerase promoter mutations are found at a high frequency in many cancer types including melanoma. However it is unclear when and if telomerase is strictly required during tumorigenesis. Here we show that melanoma can occur in the absence of telomerase. Nevertheless it is required to sustain later growth and avoid regression. Using telomerase mutant zebrafish tert / combined with two established melanoma models we found equal melanoma incidence and invasiveness as tumors became visible. Later however while WT fish develop increasing larger tumors tert / tumors stagnate growth and regress. Consistently tert / tumors showed lower cell proliferation higher apoptosis and melanocyte differentiation. We also detected an immune response to tert / tumors. Indeed tert / tumors resumed growth when transplanted to immunocompromised hosts. We propose that telomerase is required for melanoma in zebrafish albeit at later stages of progression to sustain growth while avoiding immune rejection and regression. Thus absence of telomerase restricts melanoma through tumor autonomous mechanisms cell cycle arrest apoptosis and melanocyte differentiation and a non tumor autonomous mechanisms immune rejection.			3006/1	1B	strain:AB\|age:3 month\|sex:male\|tissue:Tumor\|birth date:10.03.2021\|birth location:PEMAV IRCAN France\|death date:30.06.2021\|genotype:tert / rep1\|BioSampleModel:Model organism or animal									RNA Seq of Danio rerio : 3months male tumor	1B	1B	RNA Seq of Danio rerio : 3months male tumor			RNA-Seq	TRANSCRIPTOMIC	Oligo-dT	PAIRED	BGISEQ	BGISEQ-500	SRP426991	1B_1.fq.gz 1B_2.fq.gz	fastq fastq	10556248400.0	52781242.0	1B 1.fq.gz	0:100 1:100	A:2849865226;C:2384848330;G:2457353526;T:2864181318;N:0	100	100	2849865226	2384848330	2457353526	2864181318	SRX19650800	SRS17019452	SRA1603485	Sun Yat-sen University Cancer Center\|State Key Laboratory of Oncology in South China	Sun Yat-sen University Cancer Center Miguel Godinho Ferreira	2	0.91378	0.91775	0.13203	0.13044	0.73373	0.73342	0.51084	0.51194	100	100	B	B	biological fallback assumption	bgi	bgi	unknown	poly_a	unknown	bulk	unknown	unknown	China	2023-03-14	Adult	Adult	Cancer or Tumor	Cancer or Tumor

Advanced export

JSON shape: default, array, newline-delimited

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