期刊
BIOCHIMIE
卷 90, 期 1, 页码 73-82出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2007.07.009
关键词
telomere shortening; telomerase; crisis; genome instability; immortalization; tumorigenicity; karyotype evolution; breakage-fusion-bridge; mutator phenotype; CIN; MIN; PIN
Telomeres are required to preserve genome integrity, chromosome stability, nuclear architecture and chromosome pairing during meiosis. Given that telomerase activity is limiting or absent in most somatic tissues, shortening of telomeres during development and aging is the rule. In vitro, telomere length operates as a mechanism to prevent uncontrolled cell growth and therefore defines the proliferation potential of a cell. In vitro, in somatic cells that have lost proliferation control, shortening of telomeres becomes the main source of genome instability leading to genetic or epigenetic changes that may allow cells to become immortal and to acquire tumor phenotypes. In vivo, mice models have indisputably shown both the protective and the promoting role of very short telomeres in cancer development. In humans, although telomere shortening and other types of telomere dysfunction probably contribute to the genome instability often detected in tumors, the specific contributions of such instability to the development of cancer remain largely undetermined. (c) 2007 Elsevier Masson SAS. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据