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Inhibition of PLK4 remodels histone methylation and activates the immune response via the cGAS-STING pathway in TP53-mutated AML.

Blood - 7 Dec 2023

Man Cheuk-Him, Lam Wing, Dang Chee-Chean, Zeng Xiao-Yuan, Zheng Li-Chuan, Chan Natalie Nok-Man, Ng Ka-Lam, Chan Koon-Chuen, Kwok Tsz-Ho, Ng Timothy Chi-Chun, Leung Wing-Yan, Huen Michael Shing-Yan, Wong Carmen Chak-Lui, So Chi Wai Eric, Dou Zhixun, Goyama Susumu, Bray Mark Robert, Mak Tak Wah, Leung Anskar Yu-Hung

Abstract excerpt

Acute myeloid leukemia (AML) with TP53 mutation is one of the most lethal cancers and portends an extremely poor prognosis. Based on in silico analyses of druggable genes and differential gene expression in TP53-mutated AML, we identified pololike kinase 4 (PLK4) as a novel therapeutic target and examined its expression, regulation, pathogenetic mechanisms, and therapeutic potential in TP53-mutated AML. PLK4...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leukemia, Myeloid, Acute

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Identifiers

PMID: 37738460
DOI: 10.1182/blood.2023019782

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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