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CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (ChIP-seq)

ABSTRACT: CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (ChIP-seq)

PROVIDER: PRJNA503878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8159320.fastq.gz	Fastqsanger.gz
	SRR8159330.fastq.gz	Fastqsanger.gz
	SRR8159340.fastq.gz	Fastqsanger.gz
	SRR8159321.fastq.gz	Fastqsanger.gz
	SRR8159331.fastq.gz	Fastqsanger.gz

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CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers

Project description:CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers

| PRJNA503877 | ENA

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (Microarray)

Project description:CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (Microarray)

| PRJNA503879 | ENA

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (Microarray)

Project description:Acute Myeloid Leukemia (AML) develops due to the acquisition of mutations from multiple functional classes. Here, we demonstrate that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R), cooperate with loss of function mutations in the transcription factor CEBPA to promote acute leukemia development. Terminal myeloid differentiation in response to granulocyte colony-stimulating factor signaling requires wild type CEBPA and is blocked by mutations in CEBPA. Inhibition of the histone demethylase LSD1, restores differentiation and in combination with JAK/STAT blockade, produces significant disease response in vivo. Mutant CEBPA blocks myeloid differentiation by preventing the activation of differentiation-associated enhancers. As enhancer activation precedes promoter activation, CEBPA mutations must occur prior to CSF3R mutations to effectively block differentiation and promote leukemia formation in vivo. This study demonstrates that order-dependent oncogene interaction is a fundamental process in AML. Dissecting this process is critical for understanding disease evolution to enable the development of effective therapeutics.

2019-12-02 | GSE122161 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (ChIP-seq)

2019-12-02 | GSE122162 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - simultaneous)

2019-12-02 | GSE122164 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - orders)

2019-12-02 | GSE122163 | GEO

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - orders)

Project description:CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - orders)

| PRJNA503881 | ENA

CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - simultaneous)

Project description:CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (RNA-seq - simultaneous)

| PRJNA503880 | ENA

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

Combined Inhibition of JAK/STAT Pathway and Lysine Demethylase 1 as a Novel Therapeutic Strategy in CSF3R/CEBPA Mutant Acute Myeloid Leukemia [LSD1i ChIP-seq]

Project description:The presence of CSF3R mutations are associated with adverse outcomes in CEBPA mutant AML. Here we report that inhibitors of LSD1 reverse the mutant CEBPA-mediated differentiation blockade and exhibit synergy with JAK/STAT inhibitors.

2020-07-02 | GSE138387 | GEO

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