Alternative lengthening of telomeres, telomerase, and cancer

被引：152

作者：

Reddel, RR ^{[1
]}

机构：

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

来源：

CANCER LETTERS | 2003年 / 194卷 / 02期

基金：

英国医学研究理事会;

关键词：

telomerase; hTERT; cancer; alternative lengthening of telomeres; senescence; immortalization; ageing; Down syndrome; Werner syndrome; ataxia telangiectasia; dyskeratosis congenita;

D O I：

10.1016/S0304-3835(02)00702-4

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Telomere length may be maintained in cancer cells by telomerase or an alternative lengthening of telomeres (ALT) mechanism. Low levels of telomerase activity have been detected in some normal somatic cells and presumably some types of normal cells also have low levels of an ALT-like activity. It is hypothesized here that inherited abnormalities of these and other aspects of telomere maintenance may contribute to cancer and ageing. The telomere length maintenance mechanisms are similar in that activation of each is associated with immortalization. They may also confer other properties on cancer cells, however, and the nature of these additional properties may be different for telomerase and ALT. It is expected that these similarities and differences will have implications for prognosis and treatment. (C) 2002 Elsevier Science Ireland Ltd. All fights reserved.

引用

页码：155 / 162

页数：8

共 52 条

[1] Telomerase overexpression in K562 leukemia cells protects against apoptosis by serum deprivation and double-stranded DNA break inducing agents, but not against DNA synthesis inhibitors [J].