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MiR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [RNASeq 2]

ABSTRACT: miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [RNASeq 2]

PROVIDER: PRJNA989129 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25073706_1.fastq.gz	Fastqsanger.gz
	SRR25073706_2.fastq.gz	Fastqsanger.gz
	SRR25073707_1.fastq.gz	Fastqsanger.gz
	SRR25073707_2.fastq.gz	Fastqsanger.gz
	SRR25073708_1.fastq.gz	Fastqsanger.gz

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease

Project description:miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [scRNAseq]

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [BulkRNA 1]

Project description:miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [BulkRNA 1]

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [scRNAseq]

Project description:Complete elimination of B-cell acute lymphoblastic leukemia (B-ALL) by a risk-adapted primary treatment approach remains a clinical key objective, which fails in up to a third of patients. We hypothesized that microRNA-126, a core regulator of hematopoietic and leukemic stem cells, may resolve intra-tumor heterogeneity in B-ALL and uncover therapy-resistant subpopulations. By means of a miR-126-high signature (obtained by transducing primary human-B-all cells with a miR-126 reporter vector) and single cell RNA sequencing we identified a miR-126 derived intra tumoral heterogeneity in unmanipulated primary human B-ALL blasts

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [BulkRNA 1]

Project description:Complete elimination of B-cell acute lymphoblastic leukemia (B-ALL) by a risk-adapted primary treatment approach remains a clinical key objective, which fails in up to a third of patients. Recent evidence has implicated subpopulations of B-ALL cells with stem-like features in disease persistence. We hypothesized that microRNA-126, a core regulator of hematopoietic and leukemic stem cells, may resolve intra-tumor heterogeneity in B-ALL and uncover therapy-resistant subpopulations. We exploited patient-derived xenograft (PDX) models with B-ALL cells transduced with a miR-126 reporter allowing the prospective isolation of miR-126(high) cells for their functional and transcriptional characterization. Discrete miR-126(high) populations, often characterized by MIR126 locus de-methylation, were identified in 8/9 PDX models and showed increased repopulation potential, in vivo chemotherapy resistance and hallmarks of quiescence, inflammation and stress-response pathway activation. Cells with a miR-126(high) transcriptional profile were identified as distinct disease subpopulations by single cell RNA sequencing in diagnosis samples from adult and pediatric B-ALL. Expression of miR-126 and locus methylation were tested in several pediatric and adult B-ALL cohorts, which received standardized treatment. High microRNA-126 levels and locus de-methylation at diagnosis associate with sub-optimal response to induction chemotherapy (MRD > 0.05% at day +33 or MRD+ at day +78).

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [RNASeq 2]

Project description:Complete elimination of B-cell acute lymphoblastic leukemia (B-ALL) by a risk-adapted primary treatment approach remains a clinical key objective, which fails in up to a third of patients. Recent evidence has implicated subpopulations of B-ALL cells with stem-like features in disease persistence. We hypothesized that microRNA-126, a core regulator of hematopoietic and leukemic stem cells, may resolve intra-tumor heterogeneity in B-ALL and uncover therapy-resistant subpopulations. We exploited patient-derived xenograft (PDX) models with B-ALL cells transduced with a miR-126 reporter allowing the prospective isolation of miR-126(high) cells for their functional and transcriptional characterization. Discrete miR-126(high) populations, often characterized by MIR126 locus de-methylation, were identified in 8/9 PDX models and showed increased repopulation potential, in vivo chemotherapy resistance and hallmarks of quiescence, inflammation and stress-response pathway activation. Cells with a miR-126(high) transcriptional profile were identified as distinct disease subpopulations by single cell RNA sequencing in diagnosis samples from adult and pediatric B-ALL. Expression of miR-126 and locus methylation were tested in several pediatric and adult B-ALL cohorts, which received standardized treatment. High microRNA-126 levels and locus de-methylation at diagnosis associate with sub-optimal response to induction chemotherapy (MRD > 0.05% at day +33 or MRD+ at day +78).

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miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease

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