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 68887,SRR18218065,SRX14364509,SRS12177804,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,CG1 P2mut STABLE 5,,strain:CG1|age:133 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:23 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 5|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1,CG1 P2mut STABLE 5,CG1 P2mut STABLE 5,CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAURAAPEI-P51E3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAURAAPEI-P51E3_2.fq.gz,fastq fastq,18195264000.0,60650880.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAURAAPEI P51E3 1.fq.gz,0:150 1:150,A:4675448937;C:4456563746;G:4459950645;T:4603273696;N:26976,150,150,,,4675448937,4456563746,4459950645,4603273696,26976,SRX14364509,SRS12177804,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94521,0.94594,0.11243,0.11174,0.79551,0.79496,0.51393,0.51099,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Adult,Adult,Lymphatic System,Cardiovascular System 68888,SRR18218066,SRX14364508,SRS12177803,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,CG1 P2mut STABLE 4,,strain:CG1|age:133 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:23 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 4|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1,CG1 P2mut STABLE 4,CG1 P2mut STABLE 4,CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAATRAAPEI-P39D3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAATRAAPEI-P39D3_2.fq.gz,fastq fastq,18145191600.0,60483972.0,FCHT5GHDSXX L1 HKRDZEBmfpEAATRAAPEI P39D3 1.fq.gz,0:150 1:150,A:4669829222;C:4433244502;G:4437119015;T:4604972909;N:25952,150,150,,,4669829222,4433244502,4437119015,4604972909,25952,SRX14364508,SRS12177803,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94405,0.94389,0.11135,0.11157,0.79401,0.79385,0.50436,0.50132,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Adult,Adult,Lymphatic System,Cardiovascular System 68893,SRR18218072,SRX14364503,SRS12177798,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc 7,,strain:Tu/AB|age:41 days|sex:not collected|tissue:lymphoid|birth date:04 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 3|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB,Tu AB mMyc 7,Tu AB mMyc 7,Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAXRAAPEI-P87H3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAXRAAPEI-P87H3_2.fq.gz,fastq fastq,18002105400.0,60007018.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAXRAAPEI P87H3 1.fq.gz,0:150 1:150,A:4483057959;C:4549819065;G:4562924506;T:4406277865;N:26005,150,150,,,4483057959,4549819065,4562924506,4406277865,26005,SRX14364503,SRS12177798,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.9259,0.92681,0.09642,0.09697,0.82479,0.82546,0.50634,0.5148,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68894,SRR18218073,SRX14364502,SRS12177797,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc 6,,strain:Tu/AB|age:42 days|sex:not collected|tissue:lymphoid|birth date:03 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 2|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB,Tu AB mMyc 6,Tu AB mMyc 6,Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAWRABPEI-P75G3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAWRABPEI-P75G3_2.fq.gz,fastq fastq,18085463400.0,60284878.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAWRABPEI P75G3 1.fq.gz,0:150 1:150,A:4716166539;C:4371919988;G:4399782048;T:4597568953;N:25872,150,150,,,4716166539,4371919988,4399782048,4597568953,25872,SRX14364502,SRS12177797,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.90432,0.90596,0.06444,0.06367,0.80048,0.80095,0.51671,0.51624,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68895,SRR18218074,SRX14364501,SRS12177796,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc 5,,strain:Tu/AB|age:42 days|sex:not collected|tissue:lymphoid|birth date:03 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 1|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB,Tu AB mMyc 5,Tu AB mMyc 5,Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAVRAAPEI-P63F3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAVRAAPEI-P63F3_2.fq.gz,fastq fastq,18063312600.0,60211042.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAVRAAPEI P63F3 1.fq.gz,0:150 1:150,A:4440821008;C:4618318980;G:4635597240;T:4368548938;N:26434,150,150,,,4440821008,4618318980,4635597240,4368548938,26434,SRX14364501,SRS12177796,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.91708,0.91735,0.0319,0.0316,0.80793,0.80744,0.50004,0.5071,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68896,SRR18218075,SRX14364500,SRS12177795,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,CG1 P2mut STABLE 3,,strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 3|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1,CG1 P2mut STABLE 3,CG1 P2mut STABLE 3,CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAASRAAPEI-P27C3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAASRAAPEI-P27C3_2.fq.gz,fastq fastq,18163928100.0,60546427.0,FCHT5GHDSXX L1 HKRDZEBmfpEAASRAAPEI P27C3 1.fq.gz,0:150 1:150,A:4642188606;C:4470457895;G:4476885626;T:4574370149;N:25824,150,150,,,4642188606,4470457895,4476885626,4574370149,25824,SRX14364500,SRS12177795,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94449,0.94468,0.0858,0.0861,0.77114,0.7696,0.52498,0.52464,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Adult,Adult,Lymphatic System,Cardiovascular System 68897,SRR18218076,SRX14364499,SRS12177794,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc+P2mut 4,,strain:Tu/AB|age:28 days|sex:not collected|tissue:lymphoid|birth date:08 02 2017|death date:08 03 2017|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut2|biological replicate:Tu AB mMyc+P1mut biological replicate 4|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB,Tu AB mMyc+P2mut 4,Tu AB mMyc+P2mut 4,Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEABBRAAPEI-P40D4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEABBRAAPEI-P40D4_2.fq.gz,fastq fastq,18117791400.0,60392638.0,FCHT5GHDSXX L1 HKRDZEBmfpEABBRAAPEI P40D4 1.fq.gz,0:150 1:150,A:4565894721;C:4513701269;G:4551999162;T:4486169550;N:26698,150,150,,,4565894721,4513701269,4551999162,4486169550,26698,SRX14364499,SRS12177794,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94,0.93956,0.08699,0.08679,0.81941,0.81832,0.51722,0.51946,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Larval,Larval,Lymphatic System,Cardiovascular System 68898,SRR18218077,SRX14364498,SRS12177793,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc+P1mut 6,,strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 3|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB,Tu AB mMyc+P1mut 6,Tu AB mMyc+P1mut 6,Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEABARAAPEI-P28C4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEABARAAPEI-P28C4_2.fq.gz,fastq fastq,18034321800.0,60114406.0,FCHT5GHDSXX L1 HKRDZEBmfpEABARAAPEI P28C4 1.fq.gz,0:150 1:150,A:4518122158;C:4519676234;G:4543758117;T:4452738564;N:26727,150,150,,,4518122158,4519676234,4543758117,4452738564,26727,SRX14364498,SRS12177793,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94431,0.94437,0.10494,0.10462,0.83177,0.83037,0.51143,0.51642,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68899,SRR18218078,SRX14364497,SRS12177792,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc+P1mut 5,,strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 2|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB,Tu AB mMyc+P1mut 5,Tu AB mMyc+P1mut 5,Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAZRAAPEI-P16B4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAZRAAPEI-P16B4_2.fq.gz,fastq fastq,17750634300.0,59168781.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAZRAAPEI P16B4 1.fq.gz,0:150 1:150,A:4503506819;C:4398697723;G:4432972998;T:4415430837;N:25923,150,150,,,4503506819,4398697723,4432972998,4415430837,25923,SRX14364497,SRS12177792,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94306,0.94321,0.07511,0.0748,0.79837,0.79819,0.51326,0.50902,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68900,SRR18218079,SRX14364496,SRS12177791,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,Tu AB mMyc+P1mut 4,,strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 1|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB,Tu AB mMyc+P1mut 4,Tu AB mMyc+P1mut 4,Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAYRAAPEI-P4A4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAYRAAPEI-P4A4_2.fq.gz,fastq fastq,18063110700.0,60210369.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAYRAAPEI P4A4 1.fq.gz,0:150 1:150,A:4583950532;C:4496933352;G:4489104841;T:4493095718;N:26257,150,150,,,4583950532,4496933352,4489104841,4493095718,26257,SRX14364496,SRS12177791,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.95231,0.9534,0.12525,0.12554,0.84404,0.84323,0.52132,0.53078,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Juvenile,Juvenile,Lymphatic System,Cardiovascular System 68911,SRR18218090,SRX14364485,SRS12177780,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,CG1 P2mut STABLE 2,,strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 2|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1,CG1 P2mut STABLE 2,CG1 P2mut STABLE 2,CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAARRAAPEI-P15B3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAARRAAPEI-P15B3_2.fq.gz,fastq fastq,18103313700.0,60344379.0,FCHT5GHDSXX L1 HKRDZEBmfpEAARRAAPEI P15B3 1.fq.gz,0:150 1:150,A:4586370941;C:4481640272;G:4519408464;T:4515867439;N:26584,150,150,,,4586370941,4481640272,4519408464,4515867439,26584,SRX14364485,SRS12177780,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94376,0.94365,0.11084,0.10978,0.79847,0.79788,0.52621,0.52367,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Adult,Adult,Lymphatic System,Cardiovascular System 68912,SRR18218091,SRX14364484,SRS12177779,SRP362416,PRJNA812715,Mutant IL7R collaborates with MYC to induce T cell Acute Lymphoblastic Leukemia,PRJNA812715,Other,T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations 10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha encoded by IL7R which occur in different molecular subtypes of this disease. However it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.,,,,,CG1 P2mut STABLE 1,,strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 1|BioSampleModel:Model organism or animal,,,,,,,,,RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1,CG1 P2mut STABLE 1,CG1 P2mut STABLE 1,CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT fragmented and converted to cDNA size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.,,,RNA-Seq,TRANSCRIPTOMIC,PolyA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP362416,,,FCHT5GHDSXX_L1_HKRDZEBmfpEAAQRAAPEI-P3A3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAQRAAPEI-P3A3_2.fq.gz,fastq fastq,18068692800.0,60228976.0,FCHT5GHDSXX L1 HKRDZEBmfpEAAQRAAPEI P3A3 1.fq.gz,0:150 1:150,A:4592071905;C:4477973011;G:4471601663;T:4527019823;N:26398,150,150,,,4592071905,4477973011,4471601663,4527019823,26398,SRX14364484,SRS12177779,SRA1380603,Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab,Instituto de Medicina Molecular Joao Lobo Antunes,2,0.94814,0.94931,0.09511,0.09463,0.79756,0.79762,0.51602,0.51609,150,150,B,B,biological fallback assumption,illumina,novaseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,Portugal,2022-03-04,Adult,Adult,Lymphatic System,Cardiovascular System