metadata: run_metadata: 5 rows where devstage_curation = "Adult" and tissue

5 rows where devstage_curation = "Adult" and tissue_curation = "Lymphatic System"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	sample.alias	sample.attributes	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.Ncount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.n_mates	seqdetective.mapping_rate.mate1	seqdetective.mapping_rate.mate2	seqdetective.nofeature_rate.mate1	seqdetective.nofeature_rate.mate2	seqdetective.sparsity.mate1	seqdetective.sparsity.mate2	seqdetective.pos_strand_rate.mate1	seqdetective.pos_strand_rate.mate2	seqdetective.readlen.mate1	seqdetective.readlen.mate2	seqdetective.judgement.mate1	seqdetective.judgement.mate2	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
68887	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	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
68896	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
68911	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	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

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