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Kapsetaki, S. E.

Publications and source records attributed to Kapsetaki, S. E..

4 recordsLinked to original sources

Germline mutation rate predicts cancer mortality across 37 vertebrate species

The explanation for why some species are more susceptible to cancer than others remains an area of intense investigation. Cancer evolves in part through the accumulation of mutations and, therefore, we hypothesized that germline mutation rates would be associated with cancer prevalence and mortality across species. We collected previously published data on germline mutation rate and cancer mortality data for 37 vertebrate species. Germline mutation rate was positively correlated with cancer mortality (P = 0.008). Why animals with increased germline mutation rates die more from cancer remains an open question, however they may benefit from close monitoring for tumors due to hereditary cancer predisposition syndromes. Early diagnoses of cancer in these species may increase their chances of treatment and overall survival.

cancer biology↗

The relationship between diet, plasma glucose, and cancer prevalence across vertebrates

Could diet and mean plasma glucose concentration (MPGluC) explain the variation in cancer prevalence across species? We collected diet, MPGluC, and neoplasia data for 160 vertebrate species from existing databases. We found that MPGluC negatively correlates with cancer and neoplasia prevalence, mostly of gastrointestinal organs. Trophic level positively correlates with cancer and neoplasia prevalence even after controlling for species MPGluC. Most species with high MPGluC (50/78 species = 64.1%) were birds. Most species in high trophic levels (42/53 species = 79.2%) were reptiles and mammals. Our results may be explained by the evolution of insulin resistance in birds which selected for loss or downregulation of genes related to insulin-mediated glucose import in cells. This led to higher MPGluC, intracellular caloric restriction, production of fewer reactive oxygen species and inflammatory cytokines, and longer telomeres contributing to longer longevity and lower neoplasia prevalence in extant birds relative to other vertebrates.

cancer biology↗

Life history and cancer in birds: clutch size predicts cancer

Cancer is a disease that affects nearly all multicellular life, including birds. However, little is known about what factors explain the variance in cancer prevalence among species. Litter size is positively correlated with cancer prevalence in managed species of mammals, and larger body size, but not incubation or nestling period, is linked to tumor prevalence in wild birds. Also, birds that produce more elaborate sexual traits are expected to have fewer resources for cancer defenses and thus higher cancer prevalence. In this study, we examined whether cancer prevalence is associated with a wide variety of life history traits (clutch size, incubation length, body mass, lifespan, and the extent of sexual dimorphism) across 108 species of managed birds in 25 different zoological facilities, sanctuaries, and veterinary clinics. We found that clutch size was positively correlated with cancer and neoplasia (both benign and malignant) prevalence, even after controlling for body mass. Cancer prevalence was not associated with incubation length, body mass, lifespan, or sexual dimorphism. The positive correlations of clutch size with cancer prevalence and neoplasia prevalence suggest that there may be life-history trade-offs between reproductive investment and somatic maintenance (in the form of cancer prevention mechanisms) in managed birds.

cancer biology↗

The ecology of cancer prevalence across species: Cancer prevalence is highest in desert species and high trophic levels

The ecology in which species live and evolve likely affects their health and vulnerability to diseases including cancer. Using 14,267 necropsy records across 244 vertebrate species, we tested if animals in low productivity habitats, with large habitat range, high body temperature and weight-inferred estimates of metabolic rates, and in high trophic levels (from lowest to highest: herbivores, invertivores, primary carnivores, and secondary carnivores) are linked with having increased prevalence of neoplasia. This study found that: (1) habitat productivity negatively correlated with the prevalence of malignancy and neoplasia across tissues, and malignancy and neoplasia in gastrointestinal tissues; (2) inferred metabolic rates negatively correlated with the prevalence of neoplasia; and (3) trophic levels positively correlated with malignancy and neoplasia prevalence in both mammals and non-mammals. However, only the correlations with trophic levels remained significant after Bonferroni corrections for multiple testing. There are several mechanisms that might explain these findings, including the biomagnification of carcinogens in higher trophic levels, as well as tradeoffs between cancer suppression versus reproduction and survival in low productivity environments.

cancer biology↗