ArticleCancer research2010
Cell selection as driving force in lung and colon carcinogenesis.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Case Studies of Gastric, Lung, and Oral Cancer Connect Etiologic Agent Prevalence to Cancer Incidence.Cancer research · 2018Article
- Dynamics of cell transformation in culture and its significance for tumor development in animals.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Parameter estimation for multistage clonal expansion models from cancer incidence data: A practical identifiability analysis.PLoS computational biology · 2017Article
- Evolution of genetic instability in heterogeneous tumors.Journal of theoretical biology · 2016Article
- Article
- Field cancerisation in colorectal cancer: a new frontier or pastures past?World journal of gastroenterology · 2015Review
- Evolutionary dynamics of morphological stability in a long-term experiment with Escherichia coli.IET systems biology · 2015Article
- Cancer evolution: mathematical models and computational inference.Systematic biology · 2015Review
- Invariant Characteristics of Carcinogenesis.PloS one · 2015Article
- Heuristic modeling of carcinogenesis for the population with dichotomous susceptibility to cancer: a pancreatic cancer example.PloS one · 2014Article
- Promotion and selection by serum growth factors drive field cancerization, which is anticipated in vivo by type 2 diabetes and obesity.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Modelling the evolution of genetic instability during tumour progression.Evolutionary applications · 2013Article
- Basic equations and computing procedures for frailty modeling of carcinogenesis: application to pancreatic cancer data.Cancer informatics · 2013Article
- Analysis of apoptosis methods recently used in Cancer Research and Cell Death & Disease publications.Cell death & disease · 2012Article
- Article
- The early history of tumor virology: Rous, RIF, and RAV.Proceedings of the National Academy of Sciences of the United States of America · 2011Review
- Stable differences in intrinsic mitochondrial membrane potential of tumor cell subpopulations reflect phenotypic heterogeneity.International journal of cell biology · 2011Article
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Authors and funding
4 authors.
Funding
Abstract
Carcinogenesis is the result of mutations and subsequent clonal expansions of mutated, selectively advantageous cells. To investigate the relative contributions of mutation versus cell selection in tumorigenesis, we compared two mathematical models of carcinogenesis in two different cancer types: lung and colon. One approach is based on a population genetics model, the Wright-Fisher process, whereas the other approach is the two-stage clonal expansion model. We compared the dynamics of tumorigenesis predicted by the two models in terms of the time period until the first malignant cell appears, which will subsequently form a tumor. The mean waiting time to cancer has been calculated approximately for the evolutionary colon cancer model. Here, we derive new analytic approximations to the median waiting time for the two-stage lung cancer model and for a multistage approximation to the Wright-Fisher process. Both equations show that the waiting time to cancer is dominated by the selective advantage per mutation and the net clonal expansion rate, respectively, whereas the mutation rate has less effect. Our comparisons support the idea that the main driving force in lung and colon carcinogenesis is Darwinian cell selection.
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