Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

ABSTRACT: Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

PROVIDER: PRJNA1107972 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28903376_1.fastq.gz	Fastqsanger.gz
	SRR28903376_2.fastq.gz	Fastqsanger.gz
	SRR28903377_1.fastq.gz	Fastqsanger.gz
	SRR28903377_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

Project description:In this study, we generated mouse models of MLL-AF9-driven AML (MA9) harboring conditional alleles for Gata2 gene to precisely investigate the role of Gata2 in drug resistance and progression of MLL-rearranged (MLL-r) AML. Our findings revealed a novel mechanism for Gata2 in blunting p53 mediated apoptosis via transcriptional repression of Rassf4, a regulator of Mdm2 protein stability.

2025-05-01 | GSE266623 | GEO

Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

2025-04-30 | GSE264719 | GEO

Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

Project description:Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

| PRJNA1103845 | ENA

Anti-leukemia activity of bortezomib through GATA2-WT1 axis in acute myeloid leukemia

Project description:GATA2 is a transcription factor essential for hematopoietic differentiation and lymphatic system formation. High expression of GATA2 has been implicated in myelodysplastic syndrome and acute myeloid leukemia. Bortezomib has a good effect in MM. However, the mechanism of bortezomib possesses anti-self-renewal and leukemogenesis in AML is still unclear. Here, we reported that GATA2 and WT1 protein is degraded by bortezomib. The half-life of GATA2 mRNA was obviously shorter in Bortezomib-treated cells. Knockdown of GATA2 by small hairpin RNAs (shRNAs) has potential anti-leukemia activity in leukemic cells. Bortezomib inhibited cell proliferation and induced apoptotic death without activation of caspases pathway. Finally, bortezomib decreased xenograft tumor size in a xenograft leukemia mouse model, and prolonged the survival time in mouse C1498 AML model. Collectively, bortezomib might be a potential treatment for AML.

2021-11-14 | GSE188358 | GEO

Drug-resistant acute myeloid leukemia

Project description:Drug-resistant acute myeloid leukemia

| PRJNA828404 | ENA

Acute Myeloid Leukemia (AML) patient xenografts

Project description:Acute Myeloid Leukemia (AML) patient xenografts

| PRJNA736604 | ENA

GATA2 monoallelic expression underlies reduced penetrance in inherited GATA2- mutated MDS/AML

Project description:Although familial myelodysplasia and acute myeloid leukemia (MDS/AML) is rare, its true prevalence is likely underestimated due to wide variations in the age of onset, disease latency and outcome between and within families, with some mutation carriers remaining asymptomatic into late adulthood. Reduced penetrance is a notable feature of germline GATA2 p.Thr354Met pedigrees. In this study, we demonstrate that silencing of the wildtype (WT) GATA2 allele discriminates between symptomatic and asymptomatic carriers and is linked with allele-specific differences in DNA methylation and H3K4me3 promotor deposition, providing a molecular explanation for the clinical heterogeneity observed within a GATA2-mutated AML family.

2018-09-21 | GSE104570 | GEO

TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by rebalancing GATA2 expression [WGBS]

Project description:The myeloid transcription factor CEBPA is recurrently biallelically mutated (i.e., double mutated; CEBPADM) in acute myeloid leukemia (AML) with a combination of hypermorphic N-terminal mutations (CEBPANT), promoting expression of the leukemia-associated p30 isoform, and amorphic C-terminal mutations. CEBPADM AML features recurrent co-occurring mutations including GATA2 lesions, however insights into mechanisms governing this co-mutational spectrum are incomplete. By combining transcriptomic and epigenomic analyses of CEBPA-TET2 co-mutated patients with models thereof, we identify GATA2 as a conserved target of the CEBPA-TET2 mutational axis, providing a rationale for the mutational spectra in CEBPADM AML. Mechanistically, we suggest that elevated CEBPA levels, driven by CEBPANT, mediate recruitment of TET2 to the Gata2 distal hematopoietic enhancer thereby increasing Gata2 expression. Conversely, CEBPADM AML gains a competitive advantage through TET2 loss, by decreasing Gata2 promoter demethylation thereby rebalancing GATA2 levels. Of clinical relevance, demethylating treatment of Cebpa-Tet2 co-mutated AML restores Gata2 levels and prolongs disease latency.

2023-08-28 | GSE213860 | GEO

TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by re-balancing GATA2 expression

Project description:The myeloid transcription factor CEBPA is recurrently biallelically mutated (i.e., double mutated; CEBPADM) in acute myeloid leukemia (AML); with a combination of hypermorphic N-terminal mutations (CEBPANT), promoting expression of the leukemia-associated p30 isoform, and amorphic C-terminal mutations. CEBPADM AML features recurrent co‑occurring mutations; however, insight into the underlying mechanisms for the co-mutational spectra is incomplete. By combining transcriptomic and epigenomic analyses of data from CEBPA-TET2-co-mutant patients with experimental models thereof, we identify GATA2 as a conserved target of the CEBPA-TET2 mutational axis, providing a rationale for the mutational spectra in CEBPADM AML. Mechanistically, we suggest that elevated CEBPA levels, driven by the CEBPANT, mediate recruitment of TET2 to the GATA2 distal hematopoietic enhancer and thereby increase GATA2 expression. Conversely, CEBPADM AML gains a competitive advantage by loss of TET2; decreasing GATA2 promoter demethylation and re-balancing GATA2 levels. Further, demethylating treatment of CEBPA-TET2-co-mutant AML restores GATA2 levels, and prolongs disease latency.

2023-08-28 | GSE214224 | GEO

TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by rebalancing GATA2 expression [RNA-Seq]

2023-08-28 | GSE213821 | GEO