Abstract
We present two different mathematical models that examine the role of cellular evolution in the development and treatment of cancer. The first is a Lotka-Volterra model of an invasive cancer subjected to chemotherapy that demonstrates rapid evolution of drug-resistant phenotypes. The second model represents a major refinement of the first one with the objective of producing a simple, but realistic model of carcinogenesis. It is a consumer-resource model (consumers = normal + mutuant cells, resource = glucose). We conclude that if mutant cells are not allowed to evolve, they will not ordinarily progress to cancer. However, if accumulating mutations allow cellular evolution and successful adaptation to proliferation constraints, normal cells will develop into invasive cancer. We find this progression is possible because normal cellular populations are not at an evolutionarily stable state and so are subject to invasion by more fit phenotypes.
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