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

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

PROVIDER: PRJNA692186 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13436442.fastq.gz	Fastqsanger.gz
	SRR13436443.fastq.gz	Fastqsanger.gz
	SRR13436444.fastq.gz	Fastqsanger.gz
	SRR13436445.fastq.gz	Fastqsanger.gz
	SRR13436446.fastq.gz	Fastqsanger.gz

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

Project description: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.

2021-01-14 | GSE164838 | GEO

Single-cell DNA sequencing reveals pervasive positive selection throughout preleukemic evolution

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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.

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Effect of PML/RARA on the transcriptome of preleukemic early promyelocytes vs PML/RARA-Flt3ITD leukemic promyelocytes

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LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [preleukemic and leukemic cells]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 mice and in preleukemic cells from Sca1-TOMATO-Lmo2 mice. Tumor-bearing thymus of eleven Sca1-TOMATO-Lmo2 mice compared with thymus cells from 4 WT mice, with TOMATO-positive thymus preleukemic T cells from 5 Sca1-TOMATO-Lmo2 mice and with TOMATO-negative thymus preleukemic T cells from 5 Sca1-TOMATO-Lmo2 mice GSM2209749 - GSM220975 and GSM2209757 - GSM2209759 were re-analyzed by GSE83571 (GSM2209767 - GSM2209776).

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Project description:Hematological malignancies develop through acquisition of mutations and clonal expansion in hematopoietic stem and progenitor cells (HSPCs). However, how individual mutations perturb the entire hematopoietic system towards malignant phenotypes remains elusive. Here, we have performed single cell RNA sequencing of bone marrow HSPCs from 8 different mutant mouse models to study mutation-specific preleukemic perturbations.

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Immune stress suppresses innate immune signaling in preleukemic precursor B cells to cause leukemia

Project description:We used microarrays to investigate gene expression changes in leukemic bone marrow from Pax5+/-;Myd88+/- mice compared with bone marrow precursor B cells from WT mice and to study the effect of Myd88 downregulation in healthy Pax5+/- proB cells. The initial steps of B-cell acute lymphoblastic leukemia (B-ALL) development usually pass unnoticed in children; germline or somatic alterations affecting transcription factor genes cause the appearance of preleukemic cells still compatible with normal hematopoiesis, and preclinical studies have shown that immune stressors can trigger the malignant transformation of these otherwise silent preleukemic precursors to full-blown B-ALL. Understanding how exposure to immune stressors drives this conversion is a longstanding and unsolved challenge. Here we unveiled a specific “gene/environmental factor” interaction triggering B-ALL development. Our data show that B-ALL development falls into the category of cancers associated with dysregulation of innate immunity, which plays a driving role in the clonal evolution of pre-malignant B-cell precursors toward B-ALL following exposure to an immune stress. Transcriptional profiling of B-ALL allowed the identification of an inflammation-dependent role for Myd88 as a key player in this process. A preleukemic B-cell-autonomous role was evidenced by a significant increase in B-ALL incidence upon Myd88 dowregulation in the leukemia-prone Pax5+/- model. Likewise, early innate immune response induction by Toll-like receptor (TLR) ligation during the preleukemic phase in Pax5+/- mice resulted in a significant delay of B-ALL development. These findings identify a central role for innate immunity dysregulation in B-ALL, with important implications for the understanding and potential therapeutic targeting of the preleukemic state in children.

2023-08-10 | GSE221597 | GEO

Gene expression analysis of leukemia-initiating cells of preleukemic compound URE-/+::Msh2-/- mice

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2015-09-07 | E-GEOD-65669 | biostudies-arrayexpress

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