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Nonheritable Cellular Variability Accelerates the Evolutionary Processes of Cancer
Steven A. Frank1,2*, Marsha Rich Rosner3
1 Department of Ecology and Evolutionary Biology, University of California, Irvine, California, United States of America, 2 Department of Ecology and Evolution, University of Chicago, Chicago, Illinois, United States of America, 3 Ben May Department for Cancer Research, University of Chicago, Chicago, Illinois, United States of America

Summary: Recent cancer studies emphasize that genetic and heritable epigenetic changes drive the evolutionary rate of cancer progression and drug resistance. We discuss the ways in which nonheritable aspects of cellular variability may significantly increase evolutionary rate. Nonheritable variability arises by stochastic fluctuations in cells and by physiological responses of cells to the environment. New approaches to drug design may be required to control nonheritable variability and the evolution of resistance to chemotherapy.

Cancer progression is a series of evolutionary changes. Those changes include enhanced cellular proliferation, reduced cellular death by abrogating normal apoptotic mechanisms, greater invasiveness by increased expression of proteases, and improved colonizing ability to achieve metastasis [1]. In response to drug treatment, cancer cells often evolve resistance and continue to spread. Each evolutionary step typically proceeds by acquisition of genetic or heritable epigenetic changes in cells. When does the novel genetic change arise in an evolutionary step? By the current view, rare genetic variants arise before widespread phenotypic change. The idea is that a novel phenotype always comes from a novel genotype [2,3]. For example, rare resistant genetic variants may exist before drug treatment [4]. The drug selects those rare resistant variants, killing the other cancer

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