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