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Infection, mutation, and cancer evolution

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Abstract

An understanding of oncogenesis can be fostered by an integration of mechanistic studies with evolutionary considerations, which help explain why these mechanisms occur. This integration emphasizes infections and mutations as joint essential causes for many cancers. It suggests that infections may play a broader causal role in oncogenesis than has been generally appreciated. An evolutionary perspective also suggests that oncogenic viruses will tend to be transmitted by routes that provide infrequent opportunities for transmission, such as transmission by sexual and salivary contact. Such routes increase the intensity of natural selection for persistence within hosts, and molecular mechanisms for persistence often compromise critical barriers to oncogenesis, particularly cell cycle arrest, apoptosis, and a cap on the total number of divisions that a cell can undergo.

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Acknowledgments

The Rena Shulsky Foundation generously supported this work as part of a project to develop a unified theory of oncogenesis. John Pepper made helpful comments on this manuscript.

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Correspondence to Paul W. Ewald.

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Ewald, P.W., Swain Ewald, H.A. Infection, mutation, and cancer evolution. J Mol Med 90, 535–541 (2012). https://doi.org/10.1007/s00109-012-0891-2

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