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Mutant p53 gain of function is interwoven into the hallmarks of cancer
Author(s) -
Solomon Hilla,
Madar Shalom,
Rotter Varda
Publication year - 2011
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2988
Subject(s) - cancer , biology , mutant , mitosis , cancer research , metastasis , cancer cell , genome instability , suppressor , gain of function , cell cycle , microbiology and biotechnology , genetics , dna damage , gene , dna
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 © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.