Suppr超能文献

端粒通过诱导衰老来限制癌症生长:获得了长期以来寻求的体内证据。

Telomeres limit cancer growth by inducing senescence: long-sought in vivo evidence obtained.

作者信息

Sedivy John M

机构信息

Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, 70 Ship Street, Providence, RI 02903, USA.

出版信息

Cancer Cell. 2007 May;11(5):389-91. doi: 10.1016/j.ccr.2007.04.014.

Abstract

Cellular senescence triggered by telomere dysfunction has long been hypothesized to constitute a tumor suppression mechanism. The evidence has come primarily from in vitro cell culture studies, and more indirectly from analysis of tumor specimens. Two recent studies, published in the current issue of Cancer Cell and online at EMBO Reports, provide direct mechanistic evidence in cleverly manipulated mouse cancer models. This work shows that telomere-induced senescence is as effective as apoptosis in reducing cancer incidence and is mediated by the tumor suppressor p53.

摘要

长期以来,人们一直假设由端粒功能障碍引发的细胞衰老构成一种肿瘤抑制机制。证据主要来自体外细胞培养研究,以及对肿瘤标本的间接分析。最近发表在本期《癌细胞》以及在线发表于《EMBO报告》上的两项研究,在巧妙构建的小鼠癌症模型中提供了直接的机制证据。这项工作表明,端粒诱导的衰老在降低癌症发病率方面与细胞凋亡同样有效,并且由肿瘤抑制因子p53介导。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验