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Telomeres, stem cells, senescence, and cancer
Open accessAbstract
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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Metadata
- Authors
- Sharpless, N. E., & DePinho, R. A.
- Venue
- Journal of Clinical Investigation
- Published
- 2004-01-15
- Volume
- 113
- Issue
- 2
- Pages
- 160-168
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2093837468
- Cited by
- 473
- References
- 51
- FWCI
- 28.49
- Type
- journal article
- Language
- en
- Open access
- bronze
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