Breathing new insights into the role of mutant p53 in lung cancer

被引：5

作者：

Chen, Tianwei ^{[1
,2
]}

Ashwood, Lauren M. ^{[3
,4
]}

Kondrashova, Olga ^{[3
,4
]}

Strasser, Andreas ^{[1
,2
]}

Kelly, Gemma ^{[1
,2
]}

Sutherland, Kate D. ^{[1
,2
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia

[2] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia

[3] QIMR Berghofer Med Res Inst, Herston, Qld, Australia

[4] Univ Queensland, Brisbane, Qld, Australia

来源：

ONCOGENE | 2025年 / 44卷 / 03期

基金：

英国医学研究理事会;

关键词：

TUMOR-SUPPRESSOR P53; BH3-ONLY PROTEINS PUMA; LI-FRAUMENI-SYNDROME; DNA-BINDING; LACTIC-ACID; MOUSE MODEL; HOMOLOGOUS RECOMBINATION; GLUCOSE-METABOLISM; MISSENSE MUTATIONS; INDUCED APOPTOSIS;

D O I：

10.1038/s41388-024-03219-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The tumour suppressor gene p53 is one of the most frequently mutated genes in lung cancer and these defects are associated with poor prognosis, albeit some debate exists in the lung cancer field. Despite extensive research, the exact mechanisms by which mutant p53 proteins promote the development and sustained expansion of cancer remain unclear. This review will discuss the cellular responses controlled by p53 that contribute to tumour suppression, p53 mutant lung cancer mouse models and characterisation of p53 mutant lung cancer. Furthermore, we discuss potential approaches of targeting mutant p53 for the treatment of lung cancer.

引用

页码：115 / 129

页数：15

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