Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

ABSTRACT: The p53 inhibitor MDMX is overexpressed in the vast majority of patients with acute myeloid leukemia (AML). Utilizing hematopoietic stem cells from four non-leukemic/pre-leukemic murine models, we performed bulk transcriptomic analysis to evaluate the impact of Mdmx overexpression.

ORGANISM(S): Mus musculus

PROVIDER: GSE164838 | GEO | 2021/01/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

Project description:MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

| PRJNA692186 | ENA

Effect of depletion of MDMX (aka MDM4) on gene expression in uveal melanoma cell line MEL202

Project description:To investigate the effect of MDMX depletion on the transcriptome of MEL202 cells we established 5 derivatives either containing a doxycyline- inducible Contrl shRNA or with 4 distinct MDMX -targeting shRNAs In thee biological replicates the cells were treated with doxycycline for 48 hrs after which RNA was isolated

2022-08-25 | GSE211802 | GEO

Identification of gene expression changes in MEF cell lines with a targeted MDMX mutation that disrupts binding to CK1-alpha kinase

Project description:The goal of this experiment is to identify genes differentially expressed in MEF cell lines with a targeted MDMX mutation that prevents binding and inhibition of CK1-alpha kinase.

2020-04-07 | GSE148138 | GEO

Microarray of MDMX C462A and wildtype mice treated with acetaminophen

Project description:Microarray of MDMX C462A and wildtype mice treated with acetaminophen

| PRJNA655235 | ENA

Next Generation Sequencing based on the DNA fragment pulled down by p53 antibody (Santa Cruz, sc-126) from MCF7 wile type and MCF7 MDMX-C463A/WT cells.

Project description:Hypothesis: Based on gene chip results and further investigation, MDMX C463A/WT cells shows large portion of transcripts change at p53 dependent manner. As transcriptional factor, p53 regulates those genes could be related to DNA binding status change. ChIP-seq was used to test this hypothesis and figure out global map of p53 binding in MCF7 C463A/WT MCF7 cells by using MCF7 parental cells as reference.

2018-01-24 | GSE109481 | GEO

scRNA-Seq of MDMX C462A and wildtype mice treated with acetaminophen

Project description:scRNA-Seq of MDMX C462A and wildtype mice treated with acetaminophen

| PRJNA655236 | ENA

Progression from the preleukemic stage to acute leukemia in TAL1/SCL-LMO1 transgenic mice

Project description:The TAL1/SCL and LMO1 oncogenic transcription factors establish a pre-leukemic state by reprogramming thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Pre-TCR signaling accelerates the progression to T-cell acute lymphoblastic leukemia (T-ALL). To directly address the importance of pre-TCR signaling in driving progression to T-ALL, we leverage on Cd3-deficient mice in which pre-TCR signaling and progression through β-selection is abrogated. In the absence of pre-TCR signaling in Cd3ε-deficient SCL-LMO1 transgenic mice, T-ALL onset is delayed by 150 days. Despite the absence of pre-TCR/CD3 signaling in these mice, we show that leukemic thymocytes exhibit the gene expression profiles of thymocytes that have undergone β-selection, i.e. exhibiting a re-activation of pre-TCR-driven proliferation signature, and a down regulation of HEB/TCF12 target genes. Lastly, monoallelic deletion of Heb is sufficient to accelerate T-ALL onset in Cd3ε-deficient SCL-LMO1 transgenic mice. Together, these results underscore the role of HEB/TCF12 as a tumor suppressor in T-ALL.

2022-03-27 | GSE198506 | GEO

A Novel Cardiotoxic Mechanism for a Pervasive Global Pollutant.

Project description: Not available

| S-EPMC5282528 | biostudies-literature

Aging of preleukemic thymocytes drives CpG island hypermethylation in T-cell acute lymphoblastic leukemia [EPICarray_109TALL]

Project description:Cancer cells display DNA hypermethylation at specific CpG islands in comparison to their normal healthy counterparts, but the mechanism that drives this so-called CpG island methylator phenotype (CIMP) remains poorly understood. Here, we show that CpG island methylation in human T-cell acute lymphoblastic leukemia (T-ALL) mainly occurs at promoters of PRC2 target genes that are not expressed in normal or malignant T-cells and which display a reciprocal association with H3K27me3 binding. In addition, we found that this aberrant methylation profile shows a strong correlation with the epigenetic age of the leukemic T cells and elucidate that a similar CpG island methylation signature is gradually established in aging pre-leukemic thymocytes from CD2-Lmo2 transgenic mice. Finally, we unexpectedly uncover that this age-related CpG island hypermethylation signature is completely resistant to the FDA-approved hypomethylating agent Decitabine. Altogether, our work demonstrates that DNA methylation reflects the epigenetic history of leukemic T cells and suggests that methylation-based subtypes of human T-ALL have followed a different trajectory towards T-cell transformation, possibly mediated by differences in the self-renewing capacity of the putative T-ALL cell-of-origin. Given that the concept of preleukemic thymocytes has only been reported in T-ALL mouse models so far, we here provide, for the first time, conceptual evidence that a pre-leukemic phase might also be involved in the pathogenesis of the human disease.

2020-09-24 | GSE155333 | GEO

Aging of preleukemic thymocytes drives CpG island hypermethylation in T-cell acute lymphoblastic leukemia [ChIPmentation_TALL]

2020-09-24 | GSE155332 | GEO

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