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Cyclin degradation for cancer therapy and chemoprevention
Author(s) -
Freemantle Sarah J.,
Liu Xi,
Feng Qing,
Galimberti Fabrizio,
Blumen Steven,
Sekula David,
Kitareewan Sutisak,
Dragnev Konstantin H.,
Dmitrovsky Ethan
Publication year - 2007
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21519
Subject(s) - cancer research , cyclin , cyclin d1 , cancer , cell cycle , cell growth , apoptosis , cancer prevention , cancer cell , biology , microbiology and biotechnology , chemistry , biochemistry , genetics
Cancer is characterized by uncontrolled cell division resulting from multiple mutagenic events. Cancer chemoprevention strategies aim to inhibit or reverse these events using natural or synthetic pharmacologic agents. Ideally, this restores normal growth control mechanisms. Diverse classes of compounds have been identified with chemopreventive activity. What unites many of them is an ability to inhibit the cell cycle by specifically modulating key components. This delays division long enough for cells to respond to mutagenic damage. In some cases, damage is repaired and in others cellular damage is sufficient to trigger apoptosis. It is now known that pathways responsible for targeting G1 cyclins for proteasomal degradation can be engaged pharmacologically. Emergence of induced cyclin degradation as a target for cancer therapy and chemoprevention in pre‐clinical models is discussed in this article. Evidence for cyclin D1 as a molecular pharmacologic target and biological marker for clinical response is based on experience of proof of principle trials. J. Cell. Biochem. 102: 869–877, 2007. © 2007 Wiley‐Liss, Inc.