Review
Cancer models, genomic instability and somatic cellular Darwinian evolution
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Correspondence: Mark P Little mark.little@imperial.ac.uk
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College Faculty of Medicine, Norfolk Place, London W2 1PG, UK
Current address: Radiation Epidemiology Branch, National Cancer Institute, Executive Plaza South, 6120 Executive Boulevard MSC 7238, Bethesda, MD 20892-7238 USA
Biology Direct 2010, 5:19 doi:10.1186/1745-6150-5-19
Published: 20 April 2010Abstract
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).
Reviewers
This article was reviewed by RA Gatenby and M Kimmel.