Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236142 | GEO | 2023/08/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

2023-08-30 | GSE236136 | GEO

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).

2023-08-30 | GSE236141 | GEO

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).

2023-08-30 | GSE236138 | GEO

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

| PRJNA989124 | ENA

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

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

| PRJNA989119 | ENA

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

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

| PRJNA989129 | ENA

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]

| PRJNA989122 | ENA

Quiescent leukaemic cells account for minimal residual disease in childhood lymphoblastic leukaemia.

Project description: Not available

| S-EPMC4693965 | biostudies-literature

MiR-126 and miR-126* regulate shear-resistant firm leukocyte adhesion to human brain endothelium.

Project description:Leukocyte adhesion to brain endothelial cells, the blood-brain barrier main component, is a critical step in the pathogenesis of neuroinflammatory diseases such as multiple sclerosis (MS). Leukocyte adhesion is mediated mainly by selectins, cell adhesion molecules and chemokines induced by pro-inflammatory cytokines such as TNFα and IFNγ, but the regulation of this process is not fully clear. This study investigated the regulation of firm leukocyte adhesion to human brain endothelium by two different brain endothelial microRNAs (miRs), miR-126 and miR-126*, that are downregulated by TNFα and IFNγ in a human brain endothelial cell line, hCMEC/D3. Using a leukocyte adhesion in vitro assay under shear forces mimicking blood flow, we observed that reduction of endothelial miR-126 and miR-126* enhanced firm monocyte and T cell adhesion to hCMEC/D3 cells, whereas their increased expression partially prevented THP1, Jurkat and primary MS patient-derived PBMC firm adhesion. Furthermore, we observed that miR-126* and miR-126 downregulation increased E-selectin and VCAM1, respectively, while miR-126 overexpression reduced VCAM1 and CCL2 expression by hCMEC/D3 cells, suggesting that these miRs regulate leukocyte adhesion by modulating the expression of adhesion-associated endothelial mRNA targets. Hence, human brain endothelial miR-126 and miR-126* could be used as a therapeutic tool to reduce leukocyte adhesion and thus reduce neuroinflammation.

| S-EPMC5372244 | biostudies-literature

Is There a Role for Minimal Residual Disease Monitoring in Follicular Lymphoma in the Chemo-Immunotherapy Era?

Project description:After 25 years, evaluation of minimal residual disease (MRD) in follicular lymphoma (FL) has become a standardized technique frequently integrated into clinical trials for its consistent and independent prognostic significance. Achievement of a sustained MRD negativity is a marker of treatment sensibility that has been associated with excellent clinical outcome in terms of clinical response and progression-free survival, independently from the employed therapy. However, no survival advantages has been reported for MRD negative patients and despite the compelling results of clinical trials, MRD evaluation has currently no role in clinical practice. Ongoing clinical trials will help in clarifying the potential setting in which MRD monitoring may have a routine clinical application i.e. allowing de-escalation of standard maintenance therapy in very low risk patients. In this review the clinical implications of MRD monitoring in Rituximab-era are discussed in light of the current treatment paradigms most aimed at reducing toxicities, and the response definition that now routinely integrates PET scan.

| S-EPMC5224815 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data