p16INK4a and the control of cellular proliferative life span -: Commentary

被引：87

作者：

Huschtscha, LI ^{[1
]}

Reddel, RR ^{[1
]}

机构：

[1] Childrens Med Res Inst, Sydney, NSW 2145, Australia

来源：

CARCINOGENESIS | 1999年 / 20卷 / 06期

关键词：

D O I：

10.1093/carcin/20.6.921

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Normal somatic cells have a limited proliferative capacity in vitro: after a finite number of cell divisions they eventually enter a non-proliferative state referred to as senescence. Senescence is thought to be a major tumor suppressor mechanism, and many cancers contain cells that have escaped from senescence and become immortalized. The role of telomerase activation in immortalization is currently attracting considerable attention, but immortalization is often associated with other changes including loss of normal function of the tumor suppressor locus, INK4a/ARF Two proteins, p16(INK4a) and p14(ARF), are encoded by this locus. Here we focus on p16(INK4a) and review accumulating evidence that loss of p16(INK4a) function may be involved in escape from the normal limits on cellular proliferative life span.

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页码：921 / 926

页数：6

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