Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic landscape of adult de novo acute myeloid leukemia offers prognostic biomarkers and putative targets

ABSTRACT: Acute myeloid leukemia (AML), caused by an interplay of genetic and epigenetic alterations, is a heterogeneous hematological malignancy characterized by accumulation of proliferative clonal abnormally myeloblasts in the bone marrow and blood. Chemotherapy resistance is common, and relapses occur frequently for the majority of AML patients, indicating a strong need for better therapeutic strategies. The molecular complexity of acute myeloid leukemia (AML) presents a considerable challenge to implementation of clinical genetic testing for accurate risk stratification. Identification of better biomarkers and alternative targeted therapeutic strategies therefore remain a high priority to enable improving established stratification and guiding risk-adapted therapy decisions. RNA-sequencing offers the greatest diagnostic return, enabling identification of whole-transcriptome expression, expressed gene fusions, single nucleotide and short insertion/deletion variants, and alternative splicing information. Therefore, a total of 157 patient bone marrow samples were collected as diagnosis and subjected to RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201492 | GEO | 2022/11/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A comparative study of bone marrow and peripheral blood CD34+ myeloblasts in acute myeloid leukaemia

Project description:To examine the differences between bone marrow (BM) and peripheral blood (PB) myeloblasts in acute myeloid leukaemia (AML), we compared CD34+ myeloblasts of paired BM and peripheral blood (PB) samples from AML patients using microarray.

2008-09-30 | GSE12326 | GEO

Transcription profiling by array of human bone marrow and peripheral blood CD34+ myeloblasts in acute myeloid leukaemia

2008-10-26 | E-GEOD-12326 | biostudies-arrayexpress

Cell-cell interactome of the hematopoietic niche and its changes in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) is an aggressive cancer which causes the rapid proliferation of immature myeloid-lineage blood cells (myeloblasts) in the bone marrow. These leukemic cells receive trophic signals from the bone marrow micro-environment (BMM) in which they reside, that are essential to the initiation and maintenance of the disease. Because this is a complex and heterogeneous tissue, many aspects of this environment remain poorly characterised due to experimental hurdles. Here we performed single-cell RNA-sequencing of bone marrow aspirates from 10 AML patients across multiple key timepoints in disease progression (diagnosis, post-treatment, relapse).

2023-06-13 | GSE227903 | GEO

Search for a novel therapeutic target in myeloid leukemia

Project description:Antibody-based therapy for cancer is now one of the most successful and important strategies for treating patients with hematological malignancies. However, the lack of efficient tumor-associated antigens restricts the targeting therapy of myeloid leukemia. Analysis of the gene expression proï¬les of primary bone marrow samples from human acute myeloid leukemia (AML) patients or healthy donors was to identify and expand novel targets for the treatment of myeloid leukemias. we found that epithelial cell adhesion molecule (EpCAM) is overexpressed in patients with AML. we analyzed the gene expression proï¬les of bone marrow mononuclear cells from 2 human acute myeloid leukemia (AML) patients and 2 healthy donors using an oligonucleotide microarray, to identify up-regulated genes in AML samples comparing with healthy tissues.

2016-05-14 | E-GEOD-79605 | biostudies-arrayexpress

Proteomic and Phosphoproteomic Landscapes of Acute Myeloid Leukemia

Project description:Label-free quantitation dataset from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.

2022-03-09 | MSV000089029 | MassIVE

Proteomic and Phosphoproteomic Landscapes of Acute Myeloid Leukemia

Project description:A deep-scale proteome and phosphoproteome database from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.

2022-03-07 | MSV000089012 | MassIVE

RUNX1-ETO translocations must proceed CSF3R mutations to promote acute myeloid leukemia development

Project description:Acute myeloid leukemia (AML) is a deadly blood cancer character by an overproduction of immature myeloid cells. AML has a high degree of genetic diversity, and the presence or absence of particular genetic alterations can greatly impact prognosis. In AML, patients with CSF3R mutations exhibit high relapse rates and poor overall survival. A recent study found that 90.5% of patients with CSF3R mutations had cooccurring RUNX1-ETO (8;21), CBFB-MYH11, or CEBPA mutations7. The RUNX1-ETO and CBFB-MYH11 translocations disrupt the core binding factor complex, an important transcriptional regulator in myeloid development. In this study, we evaluated how RUNX1-ETO modifies CSF3RT618I-driven transcriptional changes to promote the production of myeloblasts in AML. We find that RUNX1-ETO accelerates CSF3R-driven oncogenesis both in vitro and in vivo. Furthermore, RUNX1-ETO impairs the ability of CSF3R to drive myeloid differentiation associated transcriptional programs resulting in the production of immature myeloblasts which characterize this disease.

2023-10-11 | GSE218829 | GEO

Sorafenib treatment of FLT3-ITD+ acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent non-responsiveness associated with a D835 mutation

Project description:Internal tandem duplication (ITD) of the fms-related tyrosine kinase-3 (FLT3) gene occurs in 30% acute myeloid leukemias (AML) and confers a poor prognosis. Thirteen relapsed or chemo-refractory FLT3-ITD+ AML patients were treated with sorafenib (200-400 mg twice daily). Twelve patients showed clearance or near clearance of bone marrow (BM) myeloblasts after 27 (range 21–84) days with evidence of differentiation of leukemia cells. The sorafenib response was lost in most patients after 72 (range 54–287) days but the FLT3 and downstream effectors remained suppressed. Four pairs patients (before sorafenib treatment and after sorafenib relapse), total eight samples from four patients at the two time-points were subjected to microarray analysis. Gene expression profiling showed that leukemia cells which have become sorafenib resistant expressed a number of genes including ALDH1A1, JAK3 and MMP15, whose functions were unknown in AML. NOD/SCID mice transplanted with leukemia cells from patients before and during sorafenib resistance recapitulated the clinical results. Both ITD and tyrosine kinase domain (TKD) mutations at D835 were identified in leukemia initiating cells (LIC) from samples before sorafenib treatment. LIC bearing the D835 mutant have expanded during sorafenib treatment and dominated during the subsequent clinical resistance. These results suggested that sorafenib have selected more aggressive sorafenib-resistant subclones carrying both FLT3-ITD and D835 mutations and might provide important leads to further improvement of treatment outcome with FLT3 inhibitors. RNA from CD33+CD34+ myeloblasts at pre-sorafenib-treatment and post-sorafenib-relapse were collected and subjected to microarray analysis

2012-02-18 | E-GEOD-35907 | biostudies-arrayexpress

Search for a novel therapeutic target in myeloid leukemia

2016-05-14 | GSE79605 | GEO

662 adult acute myeloid leukemia (AML) cases characterized on the Affymetrix Human Genome U133 Plus 2.0 Microarray

Project description:The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision-making in acute myeloid leukemia (AML). However, approximately fifty percent of AML patients, often carrying a normal karyotype, are currently unclassifiable based these established methods. Gene expression profiling has proven to be valuable for risk stratification of AML. This is a repository of 662 adult AML cases characterized on gene expression microarrays and used for different studies investigating the mechanisms underlying leukemogenesis. Bone marrow aspirates or peripheral blood samples of three independent representative cohorts of de novo AML patients, comprising 277, 256 and 129 cases respectively, were collected at diagnosis. Gene expression profiling was performed on 662 adult AML patients who have been treated according to Dutch-Belgian Hemato-Oncology Cooperative Group and the Swiss Group for Clinical Cancer Research (HOVON/SAKK) AML-04, -04A, -29, -32, -42, -42A, -43 and -92 protocols (available at http://www.hovon.nl). All patients provided written informed consent in accordance with the Declaration of Helsinki, and the study was approved by all participating institutional review boards. Blast cell purification and RNA isolation were performed as previously described (Valk et al., Prognostically Useful Gene-Expression Profiles in Acute Myeloid Leukemia, New England Journal of Medicine, 2004).

2016-06-23 | E-MTAB-3444 | biostudies-arrayexpress

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