Norman E. Sharpless, Ronald A. DePinho
J Clin Invest.
2004;
113(2):160–168
doi:10.1172/JCI20761
This article Copyright © 2004, The American Society for Clinical Investigation
Abstract
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M
ammalian 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., p16INK4a-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.
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