Putting p53 in Context

被引：1488

作者：

Kastenhuber, Edward R. ^{[1
,2
]}

Lowe, Scott W. ^{[1
,3
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Dept Canc Biol & Genet, Sloan Kettering Inst, New York, NY 10065 USA

[2] Mem Sloan Kettering Canc Ctr, Louis V Gerstner Jr Grad Sch Biomed Sci, New York, NY 10065 USA

[3] Howard Hughes Med Inst, New York, NY 10065 USA

来源：

CELL | 2017年 / 170卷 / 06期

基金：

美国国家卫生研究院;

关键词：

WILD-TYPE P53; ACUTE MYELOID-LEUKEMIA; COLORECTAL-CANCER PATIENTS; TUMOR-SUPPRESSOR P53; EMBRYONIC STEM-CELLS; LI-FRAUMENI-SYNDROME; GAIN-OF-FUNCTION; MUTANT P53; DNA-DAMAGE; IN-VIVO;

D O I：

10.1016/j.cell.2017.08.028

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：

TP53 is the most frequently mutated gene in human cancer. Functionally, p53 is activated by a host of stress stimuli and, in turn, governs an exquisitely complex anti-proliferative transcriptional program that touches upon a bewildering array of biological responses. Despite the many unveiled facets of the p53 network, a clear appreciation of how and in what contexts p53 exerts its diverse effects remains unclear. How can we interpret p53's disparate activities and the consequences of its dysfunction to understand how cell type, mutation profile, and epigenetic cell state dictate outcomes, and how might we restore its tumor-suppressive activities in cancer?

引用

页码：1062 / 1078

页数：17

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