title: Aging, cellular senescence, and cancer.
abstract: 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.
authors.affiliation: Buck Institute for Research on Aging, Novato, California 94945, USA. jcampisi@buckinstitute.org
authors.forename: Judith
authors.initials: J
authors.lastname: Campisi
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D016922:Cellular Senescence / Q000502:physiology*; D004249:DNA Damage / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D009369:Neoplasms / Q000503:physiopathology*; D013312:Stress, Physiological / Q000502:physiology