Aging, cellular senescence, and cancer

For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of functi...

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Bibliographic Details
Published inAnnual review of physiology Vol. 75; p. 685
Main Author Campisi, Judith
Format Journal Article
LanguageEnglish
Published United States 01.01.2013
Subjects
Aging - physiology
Animals
Cellular Senescence - physiology
Disease Models, Animal
DNA Damage - physiology
Humans
Neoplasms - physiopathology
Stress, Physiological - physiology
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Summary:For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
ISSN:1545-1585
DOI:10.1146/annurev-physiol-030212-183653