Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-35008

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

OTHER RELATED OMICS DATASETS IN: PRJNA151179PRJNA151165

PROVIDER: E-GEOD-35008 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-35008-analysis-methods.tsv	Tabular
	E-GEOD-35008-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-35008-configuration.xml	Xml
	E-GEOD-35008-percentile-ranks.tsv	Tabular
	E-GEOD-35008.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 60

Similar Datasets

Proteomic characterization of CD34+ CD123+ stem cells from patients with acute myeloid leukemia

Project description:The comparative characterization of hematopoietic stem cells from healthy stem cell donors and patients with acute myeloid leukemia on a proteome level has the potential to reveal differentially regulated proteins which might be candidates for specific immunotherapy target molecules. Exemplarily, we analyzed the proteome of the cytosolic and the membrane fraction of CD34 and CD123 co-expressing FACS-sorted leukemic progenitors from five patients with acute myeloid leukemia employing mass spectrometry. As a reference, CD34+CD123+ normal hematopoietic progenitor cells from five healthy stem cell donors were analyzed. In this TMT 10-plex labeling based approach 2068 proteins were identified with 256 proteins differentially regulated in one or both cellular compartments. This study demonstrates the feasibility of a mass spectrometry based proteomic approach to detect differentially expressed proteins in two compartment fractions of leukemic stem cells as compared to their healthy stem cell counterparts.

2018-02-19 | PXD008378 | Pride

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

Expression data from human hematopoietic stem and progenitor compartments from patients with acute myeloid leukemia with complex karyotype

Project description:We applied transcriptional analysis of multiple, highly fractionated stem and progenitor populations from patients with acute myeloid leukemia (AML) with complex 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. In this dataset, we include the expression data obtained from sorted hematopoietic stem and progenitor cells from patients with AML with complex karyotype.

2020-05-29 | GSE115154 | GEO

Jiao2018 - Feedback regulation in a stem cell model with acute myeloid leukaemia

Project description:This is a mathematical model describing the hematopoietic lineages with leukemia lineages, as controlled by end-product negative feedback inhibition. Variables include hematopoietic stem cells, progenitor cells, terminally differentiated HSCs, leukemia stem cells, and terminally differentiated leukemia stem cells.

2024-09-02 | BIOMD0000000898 | BioModels

Expression data in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients

Project description:Acute myeloid leukemia (AML) is a heterogeneous clonal disorder of hematopoietic stem/progenitor cells characterized by excessive proliferation and subsequent accumulation of immature myeloid blasts, leading to impaired hematopoiesis in the bone marrow (BM). The progression of AML is closely linked to the crosstalk between leukemic cells and the BM microenvironment, in particular the mesenchymal stromal cells (MSCs). We compared the mRNA expression profile of BM-MSCs from newly diagnosed AML patients (n=3), relapsed AML patients (n=3) and healthy donor controls (n=3)

2021-11-26 | GSE122917 | GEO

Defective ribosome assembly impairs leukemia progression in a murine model of acute myeloid leukemia

Project description:Despite the advanced understanding of disease mechanisms, the current therapeutic regimens fail to cure most patients with acute myeloid leukemia (AML). In the present study, we address the role of protein synthesis control in AML leukemia stem cell (LSC) function and leukemia propagation. We apply a murine model of mixed-lineage leukemia-rearranged AML to demonstrate that LSCs synthesize more proteins per hour compared with the bulk of leukemia. Using a genetic model that permits inducible and graded regulation of ribosomal subunit joining, we show that defective ribosome assembly leads to a significant survival advantage by selectively eradicating LSCs but not normal hematopoietic stem and progenitor cells. Finally, transcriptomic and proteomic analyses identify a rare subset of LSCs with immature stem cell signature and high ribosome content that underlies the resistance to defective ribosome assembly. Collectively, our study unveils a critical requirement of high protein synthesis rate for LSC function, highlighting ribosome assembly as a therapeutic target in AML.

2024-10-08 | PXD038318 | Pride

Homo sapiens

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

| PRJNA151179 | ENA

Casirati et al. Epitope Editing of Hematopoietic Stem Cells

Project description:Data for the manuscript Casirati et al. "Epitope Editing of Hematopoietic Stem Cells Enables Adoptive Immunotherapies for Acute Myeloid Leukemia"

2023-06-26 | MSV000092272 | MassIVE

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

2012-09-05 | GSE35008 | GEO

FBXO9 in Murine Inversion 16 AML

Project description:The hematopoietic system is maintained throughout life by hematopoietic stem cells that are capable of differentiation to all hematopoietic lineages. An intimate balance between self-renewal, differentiation, and quiescence is required to maintain hematopoiesis. Disruption of this balance can result in hematopoietic malignancy, including acute myeloid leukemia (AML). FBXO9, from the F-box ubiquitin E3 ligases, is down-regulated in patients with AML compared to normal bone marrow. FBXO9 is a substrate recognition component of the Skp1-Cullin-F-box (SCF)-type E3 ligase complex. FBXO9 is highly expressed in hematopoietic stem and progenitor populations, which contain the tumor-initiating population in AML. In AML patients, decrease in FBXO9 expression is most pronounced in patients with the inversion of chromosome 16 (Inv(16)), a rearrangement that generates the transcription factor fusion gene, CBFB-MYH11. To study FBXO9 in malignant hematopoiesis, we generated a conditional knockout mouse model using a novel CRISPR/Cas9 strategy. Our data shows that deletion of Fbxo9 in mice expressing Cbfb-MYH11 leads to markedly accelerated and aggressive leukemia development. In addition, we find loss of FBXO9 leads to increased proteasome expression and tumors are more sensitive to bortezomib suggesting that FBXO9 expression may predict patient response to bortezomib treatment.

2019-11-27 | PXD014387 | Pride

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