Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics profiling of human CD34+ cells from MDS bone marrow and healthy control cells

ABSTRACT: 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.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Bone Marrow, Blood

DISEASE(S): Myelodysplastic Syndrome

SUBMITTER: Zuo-Fei Yuan

LAB HEAD: Anthony A High

PROVIDER: PXD059857 | Pride | 2025-11-14

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	S13_MDS_S1-B1_1_135.d.zip	Other
	S15_HC_S1-B3_1_139.d.zip	Other
	S16_HC_S1-B4_1_141.d.zip	Other
	S17_MDS_S1-B5_1_143.d.zip	Other
	S18_MDS_S1-B6_1_145.d.zip	Other

Items per page:

1 - 5 of 51

Similar Datasets

RNA-seq of human AML, CMML and MDS CD34+ blast cells, CD4+ T cells and CD8+ T cells treated with 5-aza against untreated samples and healthy controls

Project description:This study includes 2 cohorts of samples. First cohort consists out of BM aspirates from 4 healthy individuals and 12 patients diagnosed with AML, MDS or CMML. Second cohort includes 5 healthy individuals and 17 patients diagnosed with AML, MDS or CMML. MDS and CMML patients were treated with 5-AZA on 6 cycles and samples were obtained before the treatment and 15 days after 1 and 6 rounds of treatment.

2019-12-10 | E-MTAB-8208 | biostudies-arrayexpress

miRNA expression profile analysis in myelodysplastic syndromes

Project description:The miRNA-related signaling pathways in MDS could be screened using high throughput bioinformatics analysis based on the miRNAs expression profile network. Here, we tried to identify the miRNAs-regulated pathways through a miRNA microarray in CD34+ cells from MDS patients. miRNA expression profile analysis was performed in 12 MDS patients and 6 normal controls using GeneChipÂ® miRNA 3.0 Array, and diffirential miRNAs were identified.

2016-06-30 | E-GEOD-81372 | biostudies-arrayexpress

Gene expression profile analysis in myelodysplastic syndromes

Project description:The pathogenesis-related signaling pathways in MDS could be screened using high throughput bioinformatics analysis based on the gene expression profile network. Here, we tried to identify the mRNAs-regulated pathways through a mRNA microarray in CD34+ cells from MDS patients. Gene expression profile analysis was performed in 12 MDS patients and 6 normal controls using GeneChipÂ® PrimeViewâ?¢ Human Gene Expression Array, and diffirential genes were identified.

2016-06-30 | E-GEOD-81173 | biostudies-arrayexpress

Transcription profiling of normal v early MDS v non-MDS anemia bone marrow CD34 cells to identify biomarkers of disease

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

Receptor tyrosine kinase dependent phospho-signaling networks determine cellular growth and survival in acute lymphoblastic leukemia

Project description:Receptor tyrosine kinase (RTK)-dependent signaling has been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) of childhood. However, the RTK-dependent signaling state and its interpretation with regard to biological behavior are often elusive. To decipher signaling circuits that link RTK activity with biological output in vivo, we established patient-derived xenograft ALL (PDX-ALL) models with dependencies on fms-like tyrosine kinase 3 (FLT3) and platelet-derived growth factor receptor β (PDGFRB), which were interrogated by phosphoproteomics using iTRAQ mass spectrometry. Signaling circuits were determined by receptor type and cellular context with few generic features, among which we identified group I p21-activated kinases (PAKs) as potential therapeutic targets. Growth factor stimulation markedly increased catalytic activities of PAK1 and PAK2. RNA interference (RNAi)-mediated or pharmacological inhibition of PAKs using allosteric or adenosine triphosphate (ATP)-competitive compounds attenuated cell growth and increased apoptosis in vitro. Notably, PAK1- or PAK2-directed RNAi enhanced the antiproliferative effects of the type III RTK and protein kinase C inhibitor midostaurin. Treatment of FLT3- or PDGFRB-dependent ALLs with ATP-competitive PAK inhibitors markedly decreased catalytic activities of both PAK isoforms. In FLT3-driven ALL, this effect was augmented by coadministration of midostaurin resulting in synergistic effects on growth inhibition and apoptosis. Finally, combined treatment of FLT3 D835H PDX-ALL with the ATP-competitive group I PAK inhibitor FRAX486 and midostaurin in vivo significantly prolonged leukemia progression-free survival compared with midostaurin monotherapy or control. Our study establishes PAKs as potential downstream targets in RTK-dependent ALL of childhood, the inhibition of which might help prevent the selection or acquisition of resistance mutations toward tyrosine kinase inhibitors.

2019-11-22 | PRD000749 | Pride

Myeloid malignancies with chromosome 5q deletions acquire a dependency on an intrachromosomal NF-M-NM-:B gene network

Project description:Chromosome 5q deletions (del(5q)) are common in high-risk (HR) Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML); however, the gene regulatory networks that sustain these aggressive diseases are unknown. Reduced miR-146a expression in del(5q) HR-MDS/AML and miR-146a-/- hematopoietic stem/progenitor cells (HSPC) results in TRAF6/NF-M-NM-:M-NM-^R activation. Increased survival and proliferation of HSPC from miR-146alow HR-MDS/AML is sustained by a neighboring haploid gene, SQSTM1 (p62), expressed from the intact 5q allele. Overexpression of p62 from the intact allele occurs through NF-M-NM-:B-dependent feedforward signaling mediated by miR-146a deficiency. p62 is necessary for TRAF6-mediated NF-M-NM-:B signaling, as disrupting the p62-TRAF6 signaling complex results in cell cycle arrest and apoptosis of MDS/AML cells. Thus, del(5q) HR-MDS/AML employs an intrachromosomal gene network involving loss of miR-146a and haploid overexpression of p62 via NF-M-NM-:B to sustain TRAF6/NF-M-NM-:B signaling for cell survival and proliferation. Interfering with the p62-TRAF6 signaling complex represents a therapeutic option in miR-146a-deficient and aggressive del(5q) MDS/AML. Four del(5q) MDS/AML patients with low miR-146a expression (5284, 8839, 8285, 4233) and 5 with high miR-146a expression (7957, 5534, 4688, 4982, 8412) were selected for microarray assay. RNA was reverse transcribed and labeled, and hybridized onto the GeneChip Human Gene 1.0 ST Array. A total of nine samples were included, and two groups are assigned based on miR-146a expression. Comparison comprises mRNA expression profile of low miR-146a group v.s. high miR-146a group.

2014-08-23 | E-GEOD-60649 | biostudies-arrayexpress

Expression data of ribosomal proteins from sorted hematopoietic stems cells from patients with low risk MDS.

Project description:A role for reduced ribosomal protein gene dosage in both DBA and 5q- MDS suggests that other forms of MDS might also involve altered expression of ribosomal protein genes. We used microarrays to interrogate the expression of ribosomal proteins from purified hematopoietic stems cells from patients with low risk myelodysplastic syndrome and age-matched healthy controls. Hematopoietic stem cells were sorted from 8 patients with low risk myelodysplastic syndrome and 11 age-matched healthy controls, and total RNA was hybridized to Affymetrix microarrays.

2011-08-13 | E-GEOD-30201 | biostudies-arrayexpress

Iso-seq seuqencing of leukemic pooled samples

Project description:2 samples have been prepared for ISO-seq sequencing. CD34+ blast cells from 5 MDS patients before 5-AZA treatment (GEO531A16, GEO531A13, GEO531A5, GEO531A11, GEO531A3) were pooled to generate one sample and 2 AML non-treated and 2 CMML non-treated cells (GEO531A2, GEO531A9, GEO531A6, GEO531A7) were pooled for second sample.

2019-12-10 | E-MTAB-8195 | biostudies-arrayexpress

SRSF2 is essential for hematopoiesis and its myelodysplastic syndromes-related mutations dysregulate alternative pre-mRNA splicing

Project description:We report the biological function of Srsf2 in hematopoiesis in conditional knockout mouse models. Ablation of Srsf2 in the hematopoietic lineage caused embryonic lethality, and Srsf2-deficient fetal liver cells showed significantly enhanced apoptosis and decreased hematopoietic stem/progenitor cells. Induced ablation of Srsf2 in adult Mx1Cre/ Srsf2flox/flox mice upon polyinosinic:polycytidylic acid injection demonstrated a significant decrease in lineage-/Sca+/cKit+ cells in bone marrow. To reveal the functional impact of MDS-associated mutations in SRSF2, we profiled global splicing responses on an MDS-L cell line using RASL-seq, and found that the P95H missense mutation and P95 to R102 in-frame 8 amino-acid deletion caused significant changes in alternative splicing. The affected genes were enriched in cancer development and apoptosis. These findings suggest that intact Srsf2 is essential for the functional integrity of the hematopoietic system, and its mutations are likely key driver events to MDS. MDS-L cells (in triplicate) were transfected by srsf2 shRNA only, or pTRIPZ vectors containing both srsf2 shRNA and srsf2 mutants cDNA including P95H and P95 8 amino acid deletion as well as wild-type construct, followed by Dox induction. Total RNAs were extracted and been analyzed by RASL-seq.

2015-03-01 | E-GEOD-61052 | biostudies-arrayexpress

Affymetrix SNP array data for myelodysplastic syndromes (MDS) samples

Project description:The progressive mechanism of myelodysplastic syndrome (MDS) remains unknown. We report that ROBO1 and ROBO2 are identified as novel progression-related somatic mutations using whole-exome and targeted sequencing in six of 16 (37.5%) paired MDS patients undergoing disease progression. To investigated the effect of ROBO1 or ROBO2 on ROBO1/2 CN number and LOH, we employed a Cytosan 750K chip to analyze the copy-number variations (CNVs) and loss of heterogeneity (LOH) in MDS patients with ROBO1&2 mutations. Copy number and LOH analysis of Affymetrix CytoScan 750K array was performed for 14 MDS patients with ROBO1 or ROBO2 mutations

2015-09-15 | E-GEOD-73005 | biostudies-arrayexpress