The role of senescence and immortalization in carcinogenesis
The role of senescence and immortalization in carcinogenesis
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DOI：
10.1093/carcin/21.3.477
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发表时间：
2000-03-01
期刊：
影响因子：
4.7
通讯作者：
Reddel, RR
中科院分区：
文献类型：
--
作者：
Reddel, RR
正常的体细胞在衰老之前只能分裂有限的次数。肿瘤内细胞死亡的发生和克隆进化的需要意味着，除非细胞突破衰老增殖屏障并长生不老，否则肿瘤发生需要更多的细胞分裂。因此，衰老可能是一个主要的肿瘤抑制机制。在过去的十年中，对衰老和永生的研究已经进入了癌症研究的主流。目前对这一主题感兴趣的一个主要原因是观察到大多数癌症具有激活的端粒维持机制，这是不朽的标志。研究还发现，在癌症中发生的一些最常见的基因变化在永生过程中起着关键作用。
Normal somatic cells are able to divide only a limited number of times before they become senescent. The occurrence of intratumoral cell death and the need for clonal evolution mean that many more cell divisions are required for tumorigenesis than is possible unless cells breach the senescence proliferation barrier and become immortalized. Senescence may therefore be a major tumor suppressor mechanism. During the past decade the study of senescence and immortalization has entered the mainstream of cancer research. A major reason for the current interest in this subject is the observation that most cancers have an activated telomere maintenance mechanism, a marker of immortalization. It has also been found that some of the most common genetic changes known to occur in cancer have a key role in the immortalization process.