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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE81330 | GEO | 2016/07/04

SECONDARY ACCESSION(S): PRJNA321303

REPOSITORIES: GEO

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [Affymetrix]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model We compared Gene expression profile (GEP) of murine bone marrow cells transduced with GFP, AML1-ETO, MEIS2, and AML1-ETO/MEIS2. Data from MEIS1 and AML1-ETO/MEIS1 is also included. Mouse bone marrow cells were kept in culture for 48hrs after retroviral transduction. GFP positive cells were then sorted and cells were kept for further 24 hours in culture before microarray analysis.

2016-07-04 | E-GEOD-81174 | biostudies-arrayexpress

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [Affymetrix]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model

2016-07-04 | GSE81174 | GEO

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [ChIP-Seq]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model

2016-07-04 | GSE81321 | GEO

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq mouse]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model We employed RNA-seq to assess similarities/differences among murine leukemic bone marrow samples transduced with either AML1-ETO/Meis2, AML1-ETO9a/Meis2, or AML1-ETO9a

2016-07-04 | E-GEOD-81329 | biostudies-arrayexpress

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq human]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model RNA-seq to evaluate consequence of MEIS2 Knock-down on the transcriptional profle of the t(8;21) positive Kasumi-1 cell line

2016-07-04 | E-GEOD-81328 | biostudies-arrayexpress

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq mouse]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model

2016-07-04 | GSE81329 | GEO

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq human]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model

2016-07-04 | GSE81328 | GEO

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML

Project description:MEIS2 is a novel oncogenic partner in AML1-ETO positive AML

| PRJNA321303 | ENA

A FOXO1-induced oncogenic network defines the AML1-ETO preleukemic program.

Project description:Understanding and blocking the self-renewal pathway of preleukemia stem cells could prevent acute myeloid leukemia (AML) relapse. In this study, we show that increased FOXO1 represents a critical mechanism driving aberrant self-renewal in preleukemic cells expressing the t(8;21)-associated oncogene AML1-ETO (AE). Although generally considered as a tumor suppressor, FOXO1 is consistently upregulated in t(8;21) AML. Expression of FOXO1 in human CD34+ cells promotes a preleukemic state with enhanced self-renewal and dysregulated differentiation. The DNA binding domain of FOXO1 is essential for these functions. FOXO1 activates a stem cell molecular signature that is also present in AE preleukemia cells and preserved in t(8;21) patient samples. Genome-wide binding studies show that AE and FOXO1 share the majority of their binding sites, whereby FOXO1 binds to multiple crucial self-renewal genes and is required for their activation. In agreement with this observation, genetic and pharmacological ablation of FOXO1 inhibited the long-term proliferation and clonogenicity of AE cells and t(8;21) AML cell lines. Targeting of FOXO1 therefore provides a potential therapeutic strategy for elimination of stem cells at both preleukemic and leukemic stages.

| S-EPMC5606002 | biostudies-literature

A histone acetyltransferase p300 inhibitor C646 induces cell cycle arrest and apoptosis selectively in AML1-ETO-positive AML cells.

Project description:AML1-ETO fusion protein (AE) is generated by t(8;21)(q22;q22) chromosomal translocation, which is one of the most frequently observed structural abnormalities in acute myeloid leukemia (AML) and displays a pivotal role in leukemogenesis. The histone acetyltransferase p300 promotes self-renewal of leukemia cells by acetylating AE and facilitating its downstream gene expression as a transcriptional coactivator, suggesting that p300 may be a potential therapeutic target for AE-positive AML. However, the effects of p300 inhibitors on leukemia cells and the underlying mechanisms have not been extensively investigated. In the current study, we analyzed the anti-leukemia effects of C646, a selective and competitive p300 inhibitor, on AML cells. Results showed that C646 inhibited cellular proliferation, reduced colony formation, evoked partial cell cycle arrest in G1 phase, and induced apoptosis in AE-positive AML cell lines and primary blasts isolated from leukemic mice and AML patients. Nevertheless, no significant inhibitory effects were observed in granulocyte colony-stimulating factor-mobilized normal peripheral blood stem cells. Notably, AE-positive AML cells were more sensitive to lower C646 doses than AE-negative ones. And C646-induced growth inhibition on AE-positive AML cells was associated with reduced global histone H3 acetylation and declined c-kit and bcl-2 levels. Therefore, C646 may be a potential candidate for treating AE-positive AML.

| S-EPMC3563640 | biostudies-literature

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