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

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

PROVIDER: PRJNA713329 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13926962.fastq.gz	Fastqsanger.gz
	SRR13926963.fastq.gz	Fastqsanger.gz
	SRR13926964.fastq.gz	Fastqsanger.gz
	SRR13926965.fastq.gz	Fastqsanger.gz
	SRR13926966.fastq.gz	Fastqsanger.gz

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

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

| PRJNA713326 | ENA

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

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

2022-05-23 | GSE168648 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-23 | GSE168649 | GEO

Unleashing Type-2 Dendritic Cells

Project description:Unleashing Type-2 Dendritic Cells

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life strategy

Project description:life strategy

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Double-kill mechanism of artemisinin against Plasmodium

Project description:Double-kill mechanism of artemisinin against Plasmodium

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Double-kill mechanism of artemisinin against Plasmodium

Project description:The mechanism by which artemisinin and its derivatives (ARTs) kill malaria parasites remains unclear. Haem or iron activates ARTs to produce free radicals that kill malaria parasites. However, adding iron or haem supply did not enhance, but instead attenuated, the antimalarial effect of ARTs, suggesting that the free-radical effect (FRE) is not the only antimalarial mechanism of ARTs. Here, through the single-cell RNA sequencing analysis of Plasmodium yoelii 17XNL and P. falciparum 3D7 in vivo and in vitro, we found that the sensitive stages to ARTs were associated with the expression of genes related to haem and iron (HI), DNA synthesis, antioxidation and the pentose-phosphate-pathway (PPP). Furthermore, the stages included an ART-sensitive cycle crucial for DNA synthesis that encompassed the release of iron through haem degradation to the activation of the PPP by iron. Additionally, the mechanism of haemozoin formation created a unique condition for interaction between ARTs and HI. In particular, HI can attenuate the antimalarial action of ARTs, strongly suggesting the existence of a HI-use-disturbance effect that combined with FRE to confer ARTs with a double-kill antimalarial mechanism different from the effect of iron chelators.

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Oncogenic RAS primes primary acute myeloid leukemia blasts for differentiation

Project description:RAS mutations are frequently found among AML patients, generating a constitutively active signaling protein changing cellular proliferation, differentiation and apoptosis. We previously showed that treatment of AML patients with high-dose cytarabine (HDAC) is preferentially beneficial for those with an oncogenic RAS mutation. By applying a murine AML model, we could ascribe this effect to a RAS-driven, p53-dependent induction of differentiation. Here, we sought to confirm the correlation between RAS status and differentiation of blasts obtained from AML patients. The expression signature of primary AML blasts expressing oncogenic RAS where compared to blasts with wtRAS. Blasts where obtained from peripheral blood or bone marrow samples from patients with CBFbeta-MYH11 translocations and with or without an additional NRAS point mutation. As a reference, the Kasumi-1 acute myeloid leukemia cell line was used.

2015-11-20 | E-MTAB-2090 | biostudies-arrayexpress

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