rowid,run.accession,experiment.accession,sample.accession,study.accession,bioproject,study.title,study.alias,study.type,study.abstract,study.attributes,study.PMIDs,sample.description,sample.title,sample.alias,sample.centername,sample.attributes,GEOsample.title,GEOsample.dataprocessing,GEOsample.source,GEOsample.treatmentprotocol,GEOsample.extractprotocol,GEOsample.growthprotocol,GEOsample.characteristics,GEOsample.accession,experiment.title,experiment.alias,experiment.library_name,experiment.design_description,experiment.library_construction_protocol,experiment.attributes,experiment.library_strategy,experiment.library_source,experiment.library_selection,experiment.library_layout,experiment.platform,experiment.instrument_model,experiment.spot_descriptor,experiment.study_ref,run.title,run.attributes,run.filename,run.semantic_name,run.total_bases,run.total_spots,run.alias,run.read_lengths,run.base_counts,run.r1_length,run.r2_length,run.r3_length,run.r4_length,run.Acount,run.Ccount,run.Gcount,run.Tcount,run.Ncount,run.experiment,run.pool_member,submission.accession,submission.srasource,submission.bioprojectsource,seqdetective.n_mates,seqdetective.mapping_rate.mate1,seqdetective.mapping_rate.mate2,seqdetective.nofeature_rate.mate1,seqdetective.nofeature_rate.mate2,seqdetective.sparsity.mate1,seqdetective.sparsity.mate2,seqdetective.pos_strand_rate.mate1,seqdetective.pos_strand_rate.mate2,seqdetective.readlen.mate1,seqdetective.readlen.mate2,seqdetective.judgement.mate1,seqdetective.judgement.mate2,seqdetective.judgement.reason,platform_family,instrument_generation,read_bias,selection_class,prep_kit,sc_or_bulk,tech_class,technology,tech_variant,submission.bioprojectsource.country,earliest_date,devstage_curation,devstage_curation_coarse,tissue_curation,tissue_curation_coarse 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,,,1214627731,1045617960,1070259567,1221524742,0,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,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,,,1189464447,1030660361,1055524478,1200265914,0,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,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,,,1179373951,1024313469,1050720604,1187738776,0,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,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,,,1202900253,1006105416,1022157182,1215238749,0,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,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,,,1202802143,1015451294,1025320457,1215781706,0,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,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,,,1182551057,1045032741,1067880067,1191207335,0,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,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,,,1213052369,1047508174,1069309019,1220600438,0,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,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,,,1197596235,1031109315,1057301946,1204137304,0,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,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,,,1178050199,1024865996,1046777721,1185193884,0,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,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,,,1193693228,1038160916,1064460652,1201568004,0,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,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,,,1185692334,1031585570,1050205768,1196612528,0,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,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,,,1191785539,1024344626,1050598581,1199773454,0,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,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,,,2946489343,2411825502,2477056291,2960969064,0,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,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,,,2867789187,2366678430,2438457525,2887637658,0,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,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,,,2899169569,2457980147,2528851393,2919597491,0,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,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,,,2898576858,2460872365,2527128196,2924978581,0,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,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,,,2931041183,2429723251,2502283305,2946904261,0,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,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,,,2847359136,2411906169,2481911629,2863645066,0,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,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,,,2882693797,2464129073,2535344124,2909973606,0,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,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,,,2980754877,2390812269,2448674730,2996830524,0,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,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,,,3414935292,2859787251,2916851430,3412102027,0,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,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,,,3435125429,2818006678,2880078673,3429415020,0,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,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,,,2617726378,1773416208,1829194025,2566811789,0,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,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,,,3325923130,2824746317,2889873754,3331773799,0,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,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,,,3253473957,2781714853,2829572138,3246819052,0,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,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,,,3364570176,2760126284,2813170851,3376624689,0,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,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,,,3369650885,2745871807,2821246280,3344423228,0,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,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,,,3431206764,2629189354,2672190281,3431256401,0,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,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,,,2970647072,2293859072,2357521919,2961029937,0,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,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,,,2948670507,2400698003,2461964006,2965382484,0,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,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,,,2849865226,2384848330,2457353526,2864181318,0,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