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Unleashing cell-intrinsic inflammation as a strategy to kill AML blasts

ABSTRACT: Unleashing cell-intrinsic inflammation as a strategy to kill AML blasts

PROVIDER: PRJNA713326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13927035_1.fastq.gz	Fastqsanger.gz
	SRR13927035_2.fastq.gz	Fastqsanger.gz
	SRR13927036_1.fastq.gz	Fastqsanger.gz
	SRR13927036_2.fastq.gz	Fastqsanger.gz
	SRR13927037_1.fastq.gz	Fastqsanger.gz

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Unleashing cell-intrinsic inflammation as a strategy to kill AML blasts [ChIP-seq]

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Unleashing cell-intrinsic inflammation as a strategy to kill AML blasts [ChIP-seq]

Project description:Leukemic blasts are immune cells gone awry. We hypothesized that dysregulation of inflammatory pathways contributes to the maintenance of their leukemic state and can be exploited as a cell-intrinsic, self-directed immunotherapy. To this end, we applied genome-wide screens to discover genetic vulnerabilities in acute myeloid leukemia (AML) cells that are also implicated in inflammatory pathways. We identified the immune modulator interferon regulatory factor 2 binding protein 2 (IRF2BP2) as a selective dependency in AML. We validated AML cell dependency on IRF2BP2 with genetic and protein degradation approaches in vitro and genetically in vivo. Chromatin and global gene expression studies demonstrated that IRF2BP2 represses IL1B/TNFA signaling via NF-KB, and IRF2BP2 perturbation results in an acute inflammatory state leading to AML cell death. These findings elucidate a hitherto unexplored AML dependency, reveal cell-intrinsic inflammatory signaling as a mechanism priming leukemic blasts for regulated cell death, and establish IRF2BP2-mediated transcriptional repression as a mechanism for blast survival.

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