title: Telomeres, stem cells, senescence, and cancer.
abstract: Mammalian aging occurs in part because of a decline in the restorative capacity of tissue stem cells. These self-renewing cells are rendered malignant by a small number of oncogenic mutations, and overlapping tumor suppressor mechanisms (e.g., p16(INK4a)-Rb, ARF-p53, and the telomere) have evolved to ward against this possibility. These beneficial antitumor pathways, however, appear also to limit the stem cell life span, thereby contributing to aging.
authors.affiliation: Department of Medicine and Genetics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-8212, USA. nes@med.unc.edu
authors.forename: Norman E
authors.initials: NE
authors.lastname: Sharpless
authors.forename: Ronald A
authors.initials: RA
authors.lastname: DePinho
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D016922:Cellular Senescence; D016147:Genes, Tumor Suppressor; D006801:Humans; D008954:Models, Biological; D008957:Models, Genetic; D009154:Mutation; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology*; D013234:Stem Cells / Q000473:pathology; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000648:ultrastructure*
chemical_list: D019098:Telomerase