CD34+ transriptome analysis of lower-risk MDS at risk of rapid progression
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ABSTRACT:
PROVIDER: PRJEB66515 | ENA |
REPOSITORIES: ENA
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Project description:Myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic disorders characterized by ineffective blood cell production and a high risk of progression to acute myeloid leukemia (AML). CD34+ hematopoietic stem and progenitor cells (HSPCs) play a critical role in the pathophysiology of MDS, yet the proteomic changes underlying the disease remain poorly characterized. This project focuses on performing comprehensive quantitative proteomic profiling of CD34+ cells isolated from the bone marrow of MDS patients and healthy controls. By leveraging advanced mass spectrometry and quantitative proteomics techniques, we aim to identify unbiased differences in protein expression and pathways between diseased and healthy cells. These findings will contribute to a deeper understanding of the molecular mechanisms driving MDS and may reveal potential biomarkers or therapeutic targets.
2025-11-14 | PXD059857 | Pride
Project description:CD34+ transriptome analysis of lower-risk MDS at risk of rapid progression
| PRJNA955117 | ENA
Project description:Early, low risk IPSS (International Prognostic Scoring System) myelodysplasia (MDS) is a heterogeneous disorder where the molecular and cellular haematopoietic defects are poorly understood. To gain insight into this condition, we analyzed gene expression profiles of marrow CD34+ progenitor cells from normal karyotype, low blast count MDS patients, age-matched controls and patients with non-MDS anaemia. The aim of the study was to further understanding of the cellular defect in MDS and to identify biomarkers of disease Keywords: Disease v normal
2005-08-05 | GSE2779 | GEO
Project description:Early, low risk IPSS (International Prognostic Scoring System) myelodysplasia (MDS) is a heterogeneous disorder where the molecular and cellular haematopoietic defects are poorly understood. To gain insight into this condition, we analyzed gene expression profiles of marrow CD34+ progenitor cells from normal karyotype, low blast count MDS patients, age-matched controls and patients with non-MDS anaemia. The aim of the study was to further understanding of the cellular defect in MDS and to identify biomarkers of disease Experiment Overall Design: Bone marrow (BM) CD34 cells were purified from patients with MDS, non-MDS anemia and from normal donors. Total RNA was extracted from Tri-reagent and quality verified on by capillary electrophoresis (Agilent). RNA was amplified by the Affymetrix small sample protocol. cRNA was hybridised to Affymetrix U133A chips under standard conditions. Initial data was analysed in MAS 5.0
2007-09-20 | E-GEOD-2779 | biostudies-arrayexpress
Project description:CD34+ transriptome analysis of lower-risk MDS at risk of rapid progression - set of validation samples
| PRJNA1023700 | ENA
Project description:Myelodysplastic syndromes (MDS) are heterogeneous myeloid neoplasms with an increased risk of progression to secondary acute myeloid leukemia (sAML). This study investigates the genomic correlates of disease progression in MDS by profiling active genomic regulatory regions and their transcriptional impact through H3K27ac ChIP-seq and RNA-seq analysis on CD34+ bone marrow progenitors cells isolated from a prospective cohort of 86 and 357 patients, respectively. Our analysis revealed distinct patterns of genomic region activation and transcriptional regulation across different disease stages (low-risk MDS, high-risk MDS and sAML). Unexpectedly, unsupervised clustering revealed a subset of low-risk MDS patients displaying regulatory and transcriptional profiles similar to those of high-risk MDS and sAML, highlighting early molecular events that may predispose patients to disease progression. This subset is characterized by PU.1 genomic occupancy in regions linked to immune and inflammatory responses, increased T-cell and NK activation, and a higher frequency of SRSF2 mutations. Clinically, patients in this group exhibit greater susceptibility to infections and cardiovascular events, along with an elevated risk of disease progression, resulting in a significantly reduced overall survival. Functional studies demonstrate that PU.1 inhibition suppresses MDS cell proliferation and clonogenicity, as impaired PU.1 binding inhibits the activation of key transcriptional programs involved in disease advancement. Collectively, these findings identify epigenetic factors that predispose low-risk MDS patients to progression into high-risk MDS and, ultimately, sAML. Moreover, they provide proof of concept for targeting PU.1 as a potential strategy to prevent disease progression in low-risk MDS.
2026-01-29 | GSE304224 | GEO
Project description:Myelodysplastic syndromes (MDS) are heterogeneous myeloid neoplasms with an increased risk of progression to secondary acute myeloid leukemia (sAML). This study investigates the genomic correlates of disease progression in MDS by profiling active genomic regulatory regions and their transcriptional impact through H3K27ac ChIP-seq and RNA-seq analysis on CD34+ bone marrow progenitors cells isolated from a prospective cohort of 86 and 357 patients, respectively. Our analysis revealed distinct patterns of genomic region activation and transcriptional regulation across different disease stages (low-risk MDS, high-risk MDS and sAML). Unexpectedly, unsupervised clustering revealed a subset of low-risk MDS patients displaying regulatory and transcriptional profiles similar to those of high-risk MDS and sAML, highlighting early molecular events that may predispose patients to disease progression. This subset is characterized by PU.1 genomic occupancy in regions linked to immune and inflammatory responses, increased T-cell and NK activation, and a higher frequency of SRSF2 mutations. Clinically, patients in this group exhibit greater susceptibility to infections and cardiovascular events, along with an elevated risk of disease progression, resulting in a significantly reduced overall survival. Functional studies demonstrate that PU.1 inhibition suppresses MDS cell proliferation and clonogenicity, as impaired PU.1 binding inhibits the activation of key transcriptional programs involved in disease advancement. Collectively, these findings identify epigenetic factors that predispose low-risk MDS patients to progression into high-risk MDS and, ultimately, sAML.
2026-01-29 | GSE303742 | GEO
Project description:In order to gain insight into the poorly understood pathophysiology of the myelodysplastic syndromes (MDS), we have determined the gene expression profiles of the CD34+ cells of 55 MDS patients using the Affymetrix GeneChip U133 Plus2.0 platform Keywords: Disease v normal
2006-07-01 | GSE4619 | GEO
Project description:Myelodysplastic syndromes (MDS) are heterogeneous myeloid neoplasms with an increased risk of progression to secondary acute myeloid leukemia (sAML). This study investigates the genomic correlates of disease progression in MDS by profiling active genomic regulatory regions and their transcriptional impact through H3K27ac ChIP-seq and RNA-seq analysis on CD34+ bone marrow progenitors cells isolated from a prospective cohort of 86 and 357 patients, respectively. Our analysis revealed distinct patterns of genomic region activation and transcriptional regulation across different disease stages (low-risk MDS, high-risk MDS and sAML). Unexpectedly, unsupervised clustering revealed a subset of low-risk MDS patients displaying regulatory and transcriptional profiles similar to those of high-risk MDS and sAML, highlighting early molecular events that may predispose patients to disease progression. This subset is characterized by PU.1 genomic occupancy in regions linked to immune and inflammatory responses, increased T-cell and NK activation, and a higher frequency of SRSF2 mutations. Clinically, patients in this group exhibit greater susceptibility to infections and cardiovascular events, along with an elevated risk of disease progression, resulting in a significantly reduced overall survival. Functional studies demonstrate that PU.1 inhibition suppresses MDS cell proliferation and clonogenicity, as impaired PU.1 binding inhibits the activation of key transcriptional programs involved in disease advancement. Collectively, these findings identify epigenetic factors that predispose low-risk MDS patients to progression into high-risk MDS and, ultimately, sAML. Moreover, they provide proof of concept for targeting PU.1 as a potential strategy to prevent disease progression in low-risk MDS.
2026-01-29 | GSE297914 | GEO