Telomeres, stem cells, senescence, and cancer

被引：351

作者：

Sharpless, NE ^{[1
]}

DePinho, RA

机构：

[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Sch Med, Dept Med & Genet, Chapel Hill, NC 27599 USA

[2] Harvard Univ, Sch Med, Dept Adult Oncol, Dana Farber Canc Inst,Dept Med & Genet, Boston, MA USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2004年 / 113卷 / 02期

关键词：

D O I：

10.1172/JCI200420761

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

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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页码：160 / 168

页数：9

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