Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling in the leukemic stem cell-enriched CD34+ fraction identifies target genes that predict prognosis in normal karyotype AML

ABSTRACT: Mononuclear cells from AML patients (n=46) were sorted into CD34+ and CD34- subfractions and genome-wide expression analysis was performed using Illumina BeadChip Arrays (HT12 v3). Of 2 AML samples only the CD34+ fraction could be analyzed. AML CD34+ and CD34- gene expression was compared to a large group of normal CD34+ bone marrow cells (n=31).

ORGANISM(S): Homo sapiens

PROVIDER: GSE30029 | GEO | 2011/07/19

SECONDARY ACCESSION(S): PRJNA144051

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling in the leukemic stem cell-enriched CD34+ fraction identifies target genes that predict prognosis in normal karyotype AML

Project description:Mononuclear cells from AML patients (n=46) were sorted into CD34+ and CD34- subfractions and genome-wide expression analysis was performed using Illumina BeadChip Arrays (HT12 v3). Of 2 AML samples only the CD34+ fraction could be analyzed. AML CD34+ and CD34- gene expression was compared to a large group of normal CD34+ bone marrow cells (n=31). Mononuclear cells from AML patients (n=46) were sorted into CD34+ (46) and CD34- (44) subfractions and genome-wide expression analysis was performed using Illumina BeadChip Arrays (HT12 v3). AML CD34+ and CD34- gene expression was compared to a large group of normal CD34+ bone marrow cells (n=31).

2011-07-18 | E-GEOD-30029 | biostudies-arrayexpress

TMIGD2 is a leukemic stem cell-specific surface marker in human acute myeloid leukemia

Project description:To comprehensibly understand the genes and pathways associated with TMIGD2 expression in CD34-expressing leukemia cells, RNA-seq was conducted on FACS-purified CD34+TMIGD2+ and CD34+TMIGD2- subfractions of six primary AML specimens.

2023-10-02 | GSE214487 | GEO

Identification of STAT5 target genes in human CB HSC, CMP, GMP and MEP

Project description:CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3 CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3

2011-01-22 | E-GEOD-26775 | biostudies-arrayexpress

Identification of STAT5 target genes in human CB HSC, CMP, GMP and MEP

2011-01-22 | GSE26775 | GEO

AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping features

Project description:AML with mutated NPM1 usually carries normal karyotype (NK) but it may harbor chromosomal aberrations whose significance remains unclear. We addressed this question in 631 AML patients with mutated/cytoplasmic NPM1. An abnormal karyotype (AK) was present in 93/631 cases (14.7%), the most frequent abnormalities being +8, +4, -Y, del(9q), +21. Chromosome aberrations in NPM1-mutated AML were similar to, but occurred less frequently than additional chromosome changes found in other AML with recurrent cytogenetic abnormalities according to WHO classification. Four of the 31 NPM1-mutated AML patients karyotyped at different time points had NK at diagnosis but AK at relapse: del(9q) (n=2), t(2;11) (n=1), inv(12) (n=1). NPM1-mutated AML with NK or AK showed overlapping morphological, immunophenotypic (CD34-negativity) and gene expression profile (downregulation of CD34 and upregulation of HOX genes). No difference in survival was observed among NPM1-mutated AML patients independently of whether they carried a normal or abnormal karyotype, the NPM1-mutated/FLT3-ITD negative cases showing the better prognosis. Findings in our patients point to chromosomal aberrations as secondary events, reinforce the concept that NPM1 mutation is a founder genetic lesion and indicate that NPM1-mutated AML should be clinically handled as one entity, irrespective of the karyotype.

2009-06-01 | GSE16015 | GEO

BRD9 regulates leukemic cell survival via STAT5 pathway inhibition

Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer stem cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOC3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.

2019-11-11 | PXD013245 | Pride

AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping features

2009-06-01 | E-GEOD-16015 | biostudies-arrayexpress

ExpressionPDTX

Project description:RNA Expression using Illumina HT12 v3

| EGAD00010001032 | EGA

Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with normal karyotype and healthy controls

Project description:We applied a novel approach of parallel transcriptional analysis of multiple, highly fractionated stem and progenitor populations from patients with acute myeloid leukemia (AML) and a normal karyotype. We isolated phenotypic long-term HSC (LT-HSC), short-term HSC (ST-HSC), and committed granulocyte-monocyte progenitors (GMP) from individual patients, and measured gene expression profiles of each population, and in comparison to their phenotypic counterparts from age-matched healthy controls. Bone marrow samples from AML patients with normal karyotype and age-matched healthy controls were used in this study. Hematopoietic stem and progenitor compartments were purified by multiparameter-high speed fluorescence-activated cell sorting (FACS) from CD34+ enriched bone marrow to isolate LT-HSC (Lin-/CD34+/CD38-/CD90+), ST-HSC (Lin-/CD34+/CD38-/CD90-), and GMP (Lin-/CD34+/CD38+/CD123+/CD45R+).

2012-09-05 | E-GEOD-35008 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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