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Published on: October 16, 2010
Cancer risk across mammals
Orsolya Vincze1,2,3,4, Fernando Colchero5,6,7, Jean-Francois Lemaître8
1CREEC/CANECEV, MIVEGEC (CREES), University of Montpellier, CNRS, IRD, Montpellier, France. vincze.orsolya@ecolres.hu.
Cancer mortality risk in mammals is surprisingly independent of body size and lifespan, challenging long-held theories. Carnivorous diets are linked to higher cancer risks, suggesting diet and evolution shape cancer resistance.
Area of Science:
- Evolutionary Biology
- Cancer Research
- Zoology
Background:
- Cancer is common in animals, with theories predicting higher risk in larger, longer-lived species due to more cell divisions.
- Peto's paradox highlights the lack of correlation between body size/longevity and cancer risk across species.
- Empirical data on cancer risk in diverse, non-model species is scarce.
Purpose of the Study:
- To investigate Peto's paradox by analyzing cancer-related mortality across mammalian species.
- To determine the relationship between body size, lifespan, and cancer risk in mammals.
- To explore factors influencing cancer mortality across the mammalian tree of life.
Main Methods:
- Compiled a database of cancer-related mortality from 110,148 adult zoo mammals across 191 species.
- Mapped age-controlled cancer mortality onto the mammalian evolutionary tree.
- Analyzed correlations between cancer mortality, body mass, lifespan, diet, and phylogeny.
Main Results:
- Demonstrated the widespread occurrence of cancer in mammals with significant inter-order variation in mortality.
- Revealed that cancer mortality risk is largely independent of body mass and adult lifespan across species.
- Identified a higher cancer-related mortality in carnivorous mammals, particularly those consuming other mammals.
Conclusions:
- Provided unequivocal evidence supporting the body size and longevity components of Peto's paradox.
- Highlighted the crucial role of life-history evolution in developing natural cancer resistance.
- Advanced the understanding of natural anticancer defenses and their evolutionary drivers.
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