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Telomeres, stem cells, senescence, and cancer

Norman E. Sharpless, Ronald Anthony DePinho

Journal of Clinical Investigation · 2004 · ▲ 476 citations

Telomere attrition Cellular senescence Stem-cell exhaustion

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.

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Provenance

Source: OpenAlex
DOI: 10.1172/jci20761
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Fetched: 2026-09-26 MST

Cite this

APA

Sharpless, N.E., & DePinho, R.A. (2004). Telomeres, stem cells, senescence, and cancer. <em>Journal of Clinical Investigation</em>. https://doi.org/10.1172/jci20761

Vancouver

Sharpless NE, DePinho RA. Telomeres, stem cells, senescence, and cancer. Journal of Clinical Investigation. 2004. doi:10.1172/jci20761.

BibTeX

@article{norman2004Telome, title = {Telomeres, stem cells, senescence, and cancer}, author = {Norman E. Sharpless and Ronald Anthony DePinho}, journal = {Journal of Clinical Investigation}, year = {2004}, doi = {10.1172/jci20761}, }