When mutants gain new powers: news from the mutant p53 field

被引:985
作者
Brosh, Ran [1 ]
Rotter, Varda [1 ]
机构
[1] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel
关键词
TP53; GENE-MUTATIONS; ARRAYED PRIMER EXTENSION; CELLULAR TUMOR-ANTIGEN; MURINE LEUKEMIA-VIRUS; CANCER STROMAL CELLS; HEAT-SHOCK-PROTEIN; OF-FUNCTION MUTANT; CARCINOMA IN-SITU; BREAST-CANCER; WILD-TYPE;
D O I
10.1038/nrc2693
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Ample data indicate that mutant p53 proteins not only lose their tumour suppressive functions, but also gain new abilities that promote tumorigenesis. Moreover, recent studies have modified our view of mutant p53 proteins, portraying them not as inert mutants, but rather as regulated proteins that influence the cancer cell transcriptome and phenotype. This influence is clinically manifested as association of TP53 mutations with poor prognosis and drug resistance in a growing array of malignancies. Here, we review recent studies on mutant p53 regulation, gain-of-function mechanisms, transcriptional effects and prognostic association, with a focus on the clinical implications of these findings.
引用
收藏
页码:701 / 713
页数:13
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