Infection, mutation, and cancer evolution

Ewald, Paul W.; Ewald, Holly A. Swain

doi:10.1007/s00109-012-0891-2

Cited by 30 publications

(40 citation statements)

References 52 publications

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“…Improved understanding of evolutionary biology will provide new hypotheses and new lessons for NCDs, as well as how to better deal with infectious agents [11,12]. Early stimulation of the immune defense systems, as was the norm for our ancestors, and more intelligent use of antibiotics to avoid the evolution of drug resistant bacteria are just two practical applications of evolutionary concepts in medicine and public health [13,14].…”

Section: Ancient Bodies In Modern Environmentsmentioning

confidence: 99%

The evolution of evolutionary molecular medicine

Ganten

Nesse

2012

J Mol Med

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Section: Ancient Bodies In Modern Environmentsmentioning

confidence: 99%

The evolution of evolutionary molecular medicine

Ganten

Nesse

2012

J Mol Med

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“…Alternatively, infectious agents may contribute to cancer directly by encoding proteins that compromise cellular barriers to oncogenesis, such as cellular regulation of telomerase, apoptosis, cellular adhesion or cell-cycle arrest; or cellular restraints on oncogenesis, such as control of proliferation rate [16]. These characteristics evolve particularly in intracellular pathogens not because cancer is beneficial to infectious agents but apparently because these attributes increase the ability of these pathogens to reproduce within hosts with reduced exposure to immunological destruction [17]. As obligately intracellular pathogens, viruses often replicate their genomes by stimulating host cells to proliferate as an alternative to formation and release of virions.…”

Section: Introduction To Pervasiveness Of Cancer: Evolutionary Considmentioning

confidence: 99%

“…Accordingly, the known infectious causes of human cancers are disproportionately viral (table 1). Oncogenicity has arisen independently in different viruses, which invoke different molecular mechanisms to abrogate the same cellular barriers to oncogenesis; these mechanisms and their effects of cellular proliferation and immortalization are understood in great detail (reviewed by Ewald & Swain Ewald [17]). The oncogenicity of these viruses therefore appears to result from natural selection acting on the viruses to force host cell replication, thereby enhancing the propagation of the viral genomes under the constraint of immune surveillance [16].…”

Section: Introduction To Pervasiveness Of Cancer: Evolutionary Considmentioning

confidence: 99%

Infection and cancer in multicellular organisms

Ewald

2015

Phil. Trans. R. Soc. B

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Evolutionary considerations suggest that oncogenic infections should be pervasive among animal species. Infection-associated cancers are well documented in humans and domestic animals, less commonly reported in undomesticated captive animals, and rarely documented in nature. In this paper, we review the literature associating infectious agents with cancer to evaluate the reasons for this pattern. Non-malignant infectious neoplasms occur pervasively in multicellular life, but oncogenic progression to malignancy is often uncertain. Evidence from humans and domestic animals shows that non-malignant infectious neoplasms can develop into cancer, although generally with low frequency. Malignant neoplasms could be difficult to find in nature because of a low frequency of oncogenic transformation, short survival after malignancy and reduced survival prior to malignancy. Moreover, the evaluation of malignancy can be ambiguous in nature, because criteria for malignancy may be difficult to apply consistently across species. The information available in the literature therefore does not allow for a definitive assessment of the pervasiveness of infectious cancers in nature, but the presence of infectious neoplasias and knowledge about the progression of benign neoplasias to cancer is consistent with a widespread but largely undetected occurrence.

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“…; Gatenby and Gillies ), and that infectious agents often play major roles (Bouvard et al. ; zur Hausen ; Ewald and Swain Ewald ).…”

Section: Introduction: Evolutionary Processes In Oncogenesismentioning

confidence: 99%

Toward a general evolutionary theory of oncogenesis

Ewald

2012

Evolutionary Applications

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We propose an evolutionary framework, the barrier theory of cancer, which is based on the distinction between barriers to oncogenesis and restraints. Barriers are defined as mechanisms that prevent oncogenesis. Restraints, which are more numerous, inhibit but do not prevent oncogenesis. Processes that compromise barriers are essential causes of cancer; those that interfere with restraints are exacerbating causes. The barrier theory is built upon the three evolutionary processes involved in oncogenesis: natural selection acting on multicellular organisms to mold barriers and restraints, natural selection acting on infectious organisms to abrogate these protective mechanisms, and oncogenic selection which is responsible for the evolution of normal cells into cancerous cells. The barrier theory is presented as a first step toward the development of a general evolutionary theory of cancer. Its attributes and implications for intervention are compared with those of other major conceptual frameworks for understanding cancer: the clonal diversification model, the stem cell theory and the hallmarks of cancer. The barrier theory emphasizes the practical value of distinguishing between essential and exacerbating causes. It also stresses the importance of determining the scope of infectious causation of cancer, because individual pathogens can be responsible for multiple essential causes in infected cells.

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Infection, mutation, and cancer evolution

Cited by 30 publications

References 52 publications

The evolution of evolutionary molecular medicine

The evolution of evolutionary molecular medicine

Infection and cancer in multicellular organisms

Toward a general evolutionary theory of oncogenesis

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