TY - JOUR
T1 - Telomeres, stem cells, senescence, and cancer
AU - Sharpless, Norman E.
AU - DePinho, Ronald A.
PY - 2004/1
Y1 - 2004/1
N2 - 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., 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.
AB - 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., 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.
UR - http://www.scopus.com/inward/record.url?scp=85047689866&partnerID=8YFLogxK
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U2 - 10.1172/JCI20761
DO - 10.1172/JCI20761
M3 - Review article
C2 - 14722605
AN - SCOPUS:85047689866
SN - 0021-9738
VL - 113
SP - 160
EP - 168
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 2
ER -