癌症模型、基因组不稳定性和体细胞达尔文式进化。

Cancer models, genomic instability and somatic cellular Darwinian evolution.

机构信息

Department of Epidemiology and Biostatistics, School of Public Health, Imperial College Faculty of Medicine, London, UK.

出版信息

Biol Direct. 2010 Apr 20;5:19; discussion 19. doi: 10.1186/1745-6150-5-19.

The biology of cancer is critically reviewed and evidence adduced that its development can be modelled as a somatic cellular Darwinian evolutionary process. The evidence for involvement of genomic instability (GI) is also reviewed. A variety of quasi-mechanistic models of carcinogenesis are reviewed, all based on this somatic Darwinian evolutionary hypothesis; in particular, the multi-stage model of Armitage and Doll (Br. J. Cancer 1954:8;1-12), the two-mutation model of Moolgavkar, Venzon, and Knudson (MVK) (Math. Biosci. 1979:47;55-77), the generalized MVK model of Little (Biometrics 1995:51;1278-1291) and various generalizations of these incorporating effects of GI (Little and Wright Math. Biosci. 2003:183;111-134; Little et al. J. Theoret. Biol. 2008:254;229-238).

癌症生物学被批判性地回顾，有证据表明其发展可以被模拟为体细胞达尔文进化过程。也回顾了基因组不稳定性（GI）的证据。还回顾了各种准机械致癌模型，这些模型都基于这种体细胞达尔文进化假说；特别是，阿特奇和多尔（Armitage and Doll）的多阶段模型（Br. J. Cancer 1954：8；1-12），穆尔加夫卡尔（Moolgavkar）、文曾（Venzon）和克努森（Knudson）的双突变模型（MVK）（Math. Biosci. 1979：47；55-77），利特尔（Little）的广义 MVK 模型（Biometrics 1995：51；1278-1291），以及这些模型的各种推广，这些模型纳入了 GI 的影响（Little and Wright Math. Biosci. 2003：183；111-134；Little et al. J. Theoret. Biol. 2008：254；229-238）。