Reddel Roger R
Children's Medical Research Institute, 214 Hawkesbury Road, Westmead, NSW 2145, Sydney, Australia.
Cancer Lett. 2003 May 15;194(2):155-62. doi: 10.1016/s0304-3835(02)00702-4.
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.
端粒长度可通过端粒酶或端粒替代延长（ALT）机制在癌细胞中得以维持。在一些正常体细胞中已检测到低水平的端粒酶活性，并且推测某些类型的正常细胞也具有低水平的ALT样活性。本文提出假说，认为端粒维持的这些方面以及其他方面的遗传异常可能导致癌症和衰老。端粒长度维持机制具有相似性，即每种机制的激活都与永生化相关。然而，它们也可能赋予癌细胞其他特性，并且这些额外特性的本质对于端粒酶和ALT可能有所不同。预计这些异同将对预后和治疗产生影响。
