Cesare Anthony J, Reddel Roger R
Cancer Research Unit, Children's Medical Research Institute, 214 Hawkesbury Road, Westmead, New South Wales 2145, Australia.
Mech Ageing Dev. 2008 Jan-Feb;129(1-2):99-108. doi: 10.1016/j.mad.2007.11.006. Epub 2007 Dec 8.
A substantial number of human tumors utilize a telomerase-independent telomere length maintenance mechanism referred to as alternative lengthening of telomeres (ALT). Although it is known that ALT is a telomere-specific, loss of function phenotype, which involves lengthening of telomeres by homologous recombination-mediated replication of telomeric DNA, many of the details of these processes require elucidation. Here we discuss the current literature on ALT and telomere capping, specifically focusing on how alterations in telomere capping functions may permit activation of ALT and explain the phenotypic characteristics of cells in which this occurs.
相当数量的人类肿瘤利用一种不依赖端粒酶的端粒长度维持机制，称为端粒替代延长（ALT）。尽管已知ALT是一种端粒特异性的功能丧失表型，涉及通过同源重组介导的端粒DNA复制来延长端粒，但这些过程的许多细节仍需阐明。在这里，我们讨论了目前关于ALT和端粒封端的文献，特别关注端粒封端功能的改变如何可能允许ALT的激活，并解释发生这种情况的细胞的表型特征。
