Mutant p53 gain of function is interwoven into the hallmarks of cancer

被引:52
作者
Solomon, Hilla [1 ]
Madar, Shalom [1 ]
Rotter, Varda [1 ]
机构
[1] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel
关键词
p53; proliferation; cyclin; head and neck; mouse model; oncogene addiction; angiogenesis; ras; EPITHELIAL-MESENCHYMAL TRANSITION; MOUSE MODEL; OF-FUNCTION; BREAST-CANCER; KAPPA-B; INSTABILITY; EXPRESSION; GROWTH; CELLS; MUTATIONS;
D O I
10.1002/path.2988
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cancer is viewed as being governed by several aberrant biological events defined by Weinberg and Hanahan as 'hallmarks'. In most human cancers the tumour suppressor p53 is mutated, leading to its malfunction and to the acquirement of oncogenic activities, termed 'gain of function'. This commentary links mutant p53 activities to the hallmarks of cancer, describing its involvement in resistance to apoptosis, genomic instability, aberrant cell cycle, invasion and metastasis, tumour microenvironment, and inflammation. Recent work published in The Journal of Pathology by Acin and colleagues, summarized here, reveals an interesting mechanism by which mutant p53 accelerates mitosis entry. Collectively, the growing body of evidence relating mutant p53 and the hallmarks of cancer reinforces the notion that targeting mutant p53 pathways might be beneficial for anti-cancer therapy. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
引用
收藏
页码:475 / 478
页数:4
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