Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of CD34+ CML CP or healthy donor cells

ABSTRACT: RNA-seq of CD34+ CML CP or healthy donor cells

PROVIDER: PRJEB72797 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR12721585_1.fastq.gz	Fastqsanger.gz
	ERR12721585_2.fastq.gz	Fastqsanger.gz
	ERR12721586_1.fastq.gz	Fastqsanger.gz
	ERR12721586_2.fastq.gz	Fastqsanger.gz
	ERR12721587_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

RNA-seq of CD34+ CML CP cells transduced with pL-CELF2

Project description:RNA-seq of CD34+ CML CP cells transduced with pL-CELF2

| PRJEB72798 | ENA

Transcription profiling of human CD34+ subsets in chronic phase CML and healthy individuals

Project description:A characteristic of chronic phase CML is accumulation of mature cells in the peripheral blood. It has not been determined if this expansion is explained by the CD34+ cell subset composition. We conducted flowcytometry-based cell sorting to assess the CD34+ subset composition and to retrieve the respective cells. We found a significant increase in the proportion of MEP and a decrease of HSC and GMP in patients with chronic phase CML compared to their healthy counterparts. The absolute number of HSC was similar, whereas CMP, GMP and MEP were expanded 2.8- to 7.7-fold. Gene expression analysis of CD34+ cell subsets showed, that in contrast to the normal developmental hierachy, CML HSC have a transcriptional profile which is similar to CML progenitor subsets and healthy CMP. HSC in healthy individuals show greater distance to their more mature progeny within the developmental hierarchy. As the differences between CML and healthy controls were minor at the progenitor level, we focused on the further characterization of CML HSC. 614 genes were differentially expressed, including downregulation of genes involved in adhesion and migration, regulation of the stem cell pool, and differentiation. We also found abrogation of nuclear receptors NR4A1 and NR4A3, and decreased expression of c-Jun and JunB. Re-expression of c-Jun and JunB in CD34+ cells from CML patients was achieved by co-transfection of NR4A1 and NR4A3. Moreover, we functionally corroborated a decreased adhesion capacity of the CML HSC. Taken together, these findings help to explain the hematological phenotype of CML patients in chronic phase. Experiment Overall Design: CD34+ subsets of 6 patients with chronic phase CML and 5 healthy volunteers were analysed by means of gene expression profiling with the Affymetrix HU-133A 2.0 array

2009-01-13 | E-GEOD-11889 | biostudies-arrayexpress

Bone marrow CD34+/lin- cells of patients with Chronic Phase- Chronic Myeloid Leukemia (CP-CML) after 12 months of nilotinib treatment exhibit a different expression signature compared to the diagnosis and the same cells from healthy subjects

Project description:Chronic Phase-Chronic Myeloid Leukemia (CP-CML) is defined by the presence of BCR-ABL1 fusione gene, which encodes a tyrosine kinase protein that drives the uncontrolled proliferation and survival of leukemic stem cells (LSCs). Nilotinib, a tyrosine kinase inhibitor, targets the activity of BCR-ABL1 by reducing aberrant signalling pathways which drive the regeneration of LSCs. Despite nilotinib’s action, a population of resilient LSCs persist in the bone marrow (BM) and can indeed drives relapse and progression in CML patients. Our study investigated the gene expression profiling (GEP) of BM CD34+/lin- cells from 79 CP-CML patients at diagnosis compared to the BM CD34+/lin- cells from the same patients after 12 months of nilotinib treatment, and to the normal cell counterpart from 10 donors (CTRLs). GEP analyses identified 3012 significantly differentially expressed genes. Among these, we focused on certain genes involved in crucial KEGG pathways: CML, cell cycle, JAK-STAT, PI3K-Akt, MAPK, Ras, NF-kB, and ABC transporters. We demonstrated the upregulation of several genes at diagnosis compared to both 12 months of nilotinib treatment and the CTRLs. We highlighted that certain transcriptome features characterizing the diagnosis persist after 12 months of nilotinib treatment compared to CTRLs, potentially influencing the self-renewal and survival properties of LSCs.

2025-04-02 | GSE279135 | GEO

HM450K-based DNA methylation analysis of normal and Chronic Phase-Chronic Myeloid Leukemia (CP-CML)

Project description:We analysed genome wide DNA methylation of mature (CD34-CD15+) and immature (CD34+CD15-) hematopoietic cells from patients with chronic phase CML at diagnosis. before any treatment. and compared it to their counterpart cells isolated from healthy donors.

2018-03-30 | GSE106600 | GEO

Gene expression profile at single cell level of LMPP (lymphoid-primed multipotent progenitor) cells from CP-CML and BC-CML patients.

Project description:LMPPs comprise of heterogeneous populations which are progenitors of lymphocytes and myeloid cells. We aim to identify the difference of distribution of the diverse populations from CP-CML versus BC-CML patients.

2024-09-05 | GSE276130 | GEO

The hematopoietic stem cell in chronic phase CML is characterized by a transcriptional profile resembling normal myeloid progenitor cells and reflecting loss of quiescence

Project description:We found that composition of cell subsets within the CD34+ cell population is markedly altered in chronic phase (CP) chronic myeloid leukemia (CML). Specifically, proportions and absolute cell counts of common myeloid progenitors (CMP) and megakaryocyte-erythrocyte progenitors (MEP) are significantly greater in comparison to normal bone marrow whereas absolute numbers of hematopoietic stem cells (HSC) are equal. To understand the basis for this, we performed gene expression profiling (Affymetrix HU-133A 2.0) of the distinct CD34+ cell subsets from six patients with CP CML and five healthy donors. Euclidean distance analysis revealed a remarkable transcriptional similarity between the CML patients' HSC and normal progenitors, especially CMP. CP CML HSC were transcriptionally more similar to their progeny than normal HSC to theirs, suggesting a more mature phenotype. Hence, the greatest differences between CP CML patients and normal donors were apparent in HSC including downregulation of genes encoding adhesion molecules, transcription factors, regulators of stem-cell fate and inhibitors of cell proliferation in CP CML. Impaired adhesive and migratory capacities were functionally corroborated by fibronectin detachment analysis and transwell assays, respectively. Based on our findings we propose a loss of quiescence of the CML HSC on detachment from the niche leading to expansion of myeloid progenitors.

2008-12-01 | GSE11889 | GEO

H3K27 tri-methylation signature in CML CD34+ cells

Project description:This study compares the epigenetic signatures of CD34+ cells from chronic phase chronic myeloid leukemia (CML) samples and blast phase CML samples v.s. normal CD34+ cells from cord blood and adult bone marrow samples. H3K27me3 genomic loci were detected by ChIP-seq.

2021-11-08 | GSE188241 | GEO

Chronic Myeloid Leukemia (CML), induced pluripotent stem cell (iPSC)-derived lin-CD34+CD45+ (iCD34) cell population

Project description:Analysis of lin-CD34+CD45+ (iCD34+) cell population from two normal bone marrow-derived (BM1K and BM9) iPSCs and two CML (CML15 and CML17) iPSCs . CML iCD34+ cells have characteristics similar to primary CML leukemia stem cell in patients. Results provide insight into molecular profile characterized CML iCD34 and mechanism of its maintenance and drug resistance. iCD34+ cell samples obtained from two control BM1K and BM9 iPSCs (both for the same normal donor) and CML15 and CML17 iPSCs (both from the same patient in chronic phase of CML). Each group was treated with DMSO (control) or 5 μM imatinib. The complete phenotype for iCD34+ cells: lin-CD34+CD45+CD90+CD117+CD45RA-. This population also inclyde Rhodaminelow and ALDKhigh cells.

2014-08-31 | E-GEOD-60065 | biostudies-arrayexpress

Transcriptome profiling of fenretinide-treated and untreated CD34+ cells from 4 CML patients

Project description:Imatinib, as the first-line agent of chronic myeloid leukemia (CML), is ineffective in eradicating CML stem/progenitor cells, thus unable to prevent late relapse. Here we present data indicating that fenretinide preferentially targets CD34+ CML cells and enhances the efficacy of imatinib in CML. As tested by colony forming cell assays, both number and size of total colonies derived from CD34+ CML cells were significantly reduced by fenretinide, and by combining fenretinide with imatinib. In particular, colonies derived from erythroid progenitors and those derived from more primitive pluripotent progenitor cells were highly sensitive to fenretinide/fenretinide plus immtinib. Further data showed that fenretinide was able to induce apoptosis in CD34+ CML cells which were refractory to imatinib. Through transcriptome analysis and followed by molecular validation, we further showed that apoptosis induced by fenretinide in CD34+ CML cells was mediated by complex mechanisms of stress responses, probably triggered by elevated levels of intracellular reactive oxygen species. Thus, fenretinide combines with imatinib may represent a new strategy for the treatment of CML, in which fenretinide targets primitive CD34+ CML cells whereas imatinib targets leukemic blasts. This strategy may eventually reduce the risk of relapse and probably resistant as well in CML patients.

2009-12-01 | GSE17480 | GEO

Gene expression profiling of CD34+/CD38- stem cells and CD34+/CD38+ progenitor cells from healthy control samples versus acute myeloid leukemia (AML) and chronic myeloid leukemia (CML)

Project description:In an attempt to identify novel markers and immunologic targets in leukemic stem cells (LSC) in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML), we screened samples of patients with AML, CML, and controls for expression of cell surface antigens on CD34+/CD38− and CD34+/CD38+ cells by multi-color flow cytometry. In addition, we examined mRNA expression profiles in highly purified CD34+/CD38− and CD34+/CD38+ cells by gene array- and qPCR analyses. Aberrantly expressed markers were identified in all patient cohorts examined.

2020-09-21 | GSE138883 | 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