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Senescence As an Anticancer Mechanism

Peter J. Hornsby

From the Department of Physiology and Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX

Address reprint requests to Peter J. Hornsby, PhD, University of Texas Health Science Center, 15355 Lambda Dr, STCBM Bldg, San Antonio, TX 78245; e-mail: hornsby{at}uthscsa.edu

Senescence was originally described as a terminal nondividing state of normal human cells reached after many cell divisions in culture. The cause was shown to be shortening of telomeres, leading to telomere dysfunction and cell cycle arrest. Subsequently, a more rapid, nontelomere-dependent form of senescence, often termed stress-induced premature senescence, was described. Mostly importantly, it occurs in response to activated oncogene products. Oncogene-induced senescence has been shown to play a role in tumor suppression in vivo; it does not seem to involve changes in telomeres. A second phenomenon that plays a role in tumor suppression, which does involve progressive telomere shortening, is crisis, the state that cells reach when cell cycle checkpoints are impaired and cells can no longer respond to telomere shortening or oncogene activation by entering senescence. These two processes, oncogene-induced senescence and telomere-based crisis, exert powerful anticancer effects.

Supported in part by Grants No. AG12287 and AG20752 from the National Institute on Aging and by a Senior Scholar Award from the Ellison Medical Foundation.

Author's disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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