Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RAS Pathway–Mutated Chronic Myelomonocytic Leukemia at the Single Cell Level

ABSTRACT: RAS Pathway–Mutated Chronic Myelomonocytic Leukemia at the Single Cell Level

PROVIDER: PRJNA903476 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22351026.fastq.gz	Fastqsanger.gz
	SRR22351027.fastq.gz	Fastqsanger.gz
	SRR22351028_1.fastq.gz	Fastqsanger.gz
	SRR22351028_2.fastq.gz	Fastqsanger.gz
	SRR22351029_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 92

Similar Datasets

RAS Pathway–Mutated Chronic Myelomonocytic Leukemia at the Single Cell Level

Project description:RAS pathway mutations, which are present in 30% of patients with chronic myelomonocytic leukemia (CMML) at diagnosis, confer a high risk of resistance to and progression after hypomethylating agent (HMA) therapy, the current standard of care for the disease. Using single-cell, multi-omics technologies, we sought to dissect the biological mechanisms underlying the initiation and progression of RAS pathway–mutated CMML. We found that RAS pathway mutations induced the transcriptional reprogramming of hematopoietic stem and progenitor cells (HSPCs), which underwent proliferation and monocytic differentiation in response to cell-intrinsic and -extrinsic inflammatory signaling that also impaired immune cells’ functions. HSPCs expanded at disease progression and relied on the NF-KB pathway effector MCL1 to maintain their survival, which explains why patients with RAS pathway–mutated CMML do not benefit from BCL2 inhibitors such as venetoclax. Our study has implications for developing therapies to improve the survival of patients with RAS pathway–mutated CMML.

2024-04-21 | GSE218390 | GEO

Transcriptome of chronic myelomonocytic leukemia

Project description:We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of peripheral blood mononuclear cells of patients with chronic myelomonocytic leukemia.

2020-08-14 | GSE156209 | GEO

Transcriptome of chronic myelomonocytic leukemia

Project description:Transcriptome of chronic myelomonocytic leukemia

| PRJNA657050 | ENA

Inhibition of EGFR signaling downregulates K-RAS mutated activity

Project description:Inhibition of EGFR signaling downregulates K-RAS mutated activity

| PRJNA450257 | ENA

Transcriptome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

Project description:We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of bone marrow mononuclear cells of patients with chronic myelomonocytic leukemia.

2022-02-21 | GSE159543 | GEO

Oncogenic and microenvironmental signals drive cell type-specific apoptosis resistance in juvenile myelomonocytic leukemia

Project description:Juvenile myelomonocytic leukemia (JMML) is caused by constitutively activated RAS signalling and is characterized by increased proliferation and predominant myelomonocytic differentiation of hematopoietic cells. Using Mx-Cre;PTPN11D61Y mice, which reflect human JMML, we show that RAS pathway activation affects apoptosis signalling through cell type-dependent regulation of BCL-2 family members. Apoptosis resistance observed in monocytes and granulocytes was mediated by overexpression of the anti-apoptotic and down-regulation of the pro-apoptotic members of the BCL-2 family. Two anti-apoptotic proteins, BCL-XL and MCL-1, were directly regulated by the oncogenic RAS signalling but in addition were influenced by microenvironmental signals. While BCL-XL and BCL-2 were required for the survival of monocytes, MCL-1 was essential for neutrophils. Interestingly, stem and progenitor cells expressing the oncogenic PTPN11 mutant did not display any increased apoptosis resistance. BCL-XL inhibition was the most effective in killing myeloid cells in vitro but was not sufficient to completely resolve myeloproliferation in vivo.

2025-05-07 | PXD055845 | Pride

Cell type-specific apoptosis resistance in juvenile myelomonocytic leukemia

Project description:Juvenile myelomonocytic leukemia (JMML) is caused by constitutively activated RAS signaling. Activation of the RAS pathway in the JMML mouse model (MxCre;Ptpn11D61Y) affects apoptosis signaling by regulating BCL-2 family members through oncogenic and microenvironemtal signals, in a cell type-dependent manner. Apoptosis resistance mediated by overexpression of anti-apoptotic and downregulation of pro-apoptotic BCL-2 family members was observed in monocytes and granulocytes.

2025-03-19 | GSE277667 | GEO

Epigenome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

Project description:We report the chromatin characteristics of human chronic myelomonocytic leukemia by performing chromatin immunoprecipitation sequencing of histone modifications (ChIP-seq), immunoprecipitation sequencing of (hydroxy-)methylated residues (DIP-seq), and transposase accessibility sequencing (ATAC-seq) of bone marrow mononuclear cells of patients with chronic myelomonocytic leukemia.

2022-02-21 | GSE159886 | GEO

Genome-wide gene expression analysis in RAS-mutated cells with EZH2 inactivation

Project description:EZH2 was inactivated by shRNA in the RAS-mutated HL-60 acute myeloid leukemia cell line. RNA-seq genome wide expression profiling was used to screen for genes deregulated by EZH2 inactivation within this setting.

2023-05-07 | GSE150029 | GEO

Functional heterogeneity exceeds genetic heterogeneity in chronic myelomonocytic leukemia

Project description:The respective role of genetic and epigenetic heterogeneity in the functional diversity of cells that compose human malignancies remains poorly understood. This question is addressed in chronic myelomonocytic leukemia (CMML), a myeloid neoplasm in which clinical diversity contrasts with a limited genetic heterogeneity. By reprogramming CMML-patient and healthy donor CD34-positive cells, we generated induced pluripotent cell clones (iPSC). In one of the patients, we captured a part of the genetic heterogeneity of the leukemic clone and analyzed five iPSCs with two distinct genetic backgrounds, i.e. with and without KRASG12D mutation. Hematopoietic differentiation of these clones recapitulated the main features of the patient disease, including overproduction of granulomonocytes and dysmegakaryopoiesis. These analyses also disclosed significant discrepancies in the behavior as well as the DNA methylation pattern of hematopoietic cells derived from iPSCs with similar genetic background. Introduction of SRSF2P95H mutation in a KRAS-mutated iPSC partially suppressed the functional and epigenetic gap with the other KRAS-mutated clone. Despite the similar functional behavior of these two clones, only the SRSF2P95H clone responded to low doses of the hypomethylating agent decitabine by restoration of a more balanced production of hematopoietic cells. These analyses unravel additional levels of intraclonal heterogeneity beyond the coding mutations, which may also modulate individual cell response to treatment.

2020-04-14 | GSE114115 | GEO

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