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P53: An ubiquitous target of anticancer drugs
Author(s) -
Blagosklonny Mikhail V.
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.10158
Subject(s) - dna damage , apoptosis , cell cycle checkpoint , suppressor , cancer research , senescence , cell cycle , proteasome , cell growth , function (biology) , biology , dna repair , programmed cell death , cancer cell , microbiology and biotechnology , cancer , dna , genetics
Abstract The p53 tumor suppressor can induce growth arrest, apoptosis and cell senescence. Not surprisingly, p53 is an appealing target for therapeutic intervention. Although current anticancer agents do not directly interact with p53, these agents (including DNA damaging drugs, antimetabolites, microtubule‐active drugs and inhibitors of the proteasome) cause accumulation of wt p53. Depending on the p53 status of cancer cells, diverse therapeutic strategies are under development. These include pharmacological rescue of mutant p53 function and reactivation of wt p53 in E6‐expressing cells. For protection of normal cells, strategies range from abrogation of wt p53 induction, thereby decreasing the toxicity of DNA damaging agents, to activation of wt p53‐dependent checkpoints, thereby protecting cells against cell cycle‐dependent therapeutics. © 2001 Wiley‐Liss, Inc.