Telomeres, stem cells, senescence, and cancer
Norman E. Sharpless, Ronald A. DePinho
Norman E. Sharpless, Ronald A. DePinho
Published January 15, 2004
Citation Information: J Clin Invest. 2004;113(2):160-168. https://doi.org/10.1172/JCI20761.
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Perspective Series

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., 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.

Authors

Norman E. Sharpless, Ronald A. DePinho

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Figure 2

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Telomere structure. Telomeres are present at chromosome ends. They consi...
Telomere structure. Telomeres are present at chromosome ends. They consist of linear arrays of repeat sequences that are 5–15 kb in humans but considerably larger in mice. Telomeres also harbor a G-rich 3′ overhang that is important for the adoption of proper secondary structure.