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Cancer models, genomic instability and somatic cellular Darwinian evolution

Overview of attention for article published in Biology Direct, April 2010
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Title
Cancer models, genomic instability and somatic cellular Darwinian evolution
Published in
Biology Direct, April 2010
DOI 10.1186/1745-6150-5-19
Pubmed ID
Authors

Mark P Little

Abstract

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).

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 93 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 6 6%
United Kingdom 2 2%
Germany 1 1%
France 1 1%
Brazil 1 1%
Portugal 1 1%
Mexico 1 1%
Italy 1 1%
Unknown 79 85%

Demographic breakdown

Readers by professional status Count As %
Researcher 25 27%
Student > Ph. D. Student 18 19%
Student > Bachelor 9 10%
Student > Master 9 10%
Student > Postgraduate 7 8%
Other 16 17%
Unknown 9 10%
Readers by discipline Count As %
Agricultural and Biological Sciences 42 45%
Medicine and Dentistry 13 14%
Biochemistry, Genetics and Molecular Biology 7 8%
Physics and Astronomy 5 5%
Pharmacology, Toxicology and Pharmaceutical Science 4 4%
Other 11 12%
Unknown 11 12%