Rapid gene evolution may explain why whales and dolphins don't get cancer

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Rapid evolution of genes that suppress the development of tumours may explain why cetaceans - which include whales and dolphins - don't get cancer, according to international scientists. They compared the genetic code of various whale and dolphin species with the code from several land mammals, including humans, and found that tumour suppressing genes have evolved up to 2.4 times faster in the marine mammals. They also found that 71 different genes were more likely to have duplicated in cetaceans, including 11 genes linked to longevity. These genetic changes may help explain why cetaceans don't get cancer like we do, the scientists say.

Media release

From: The Royal Society

Positive selection and gene duplications in tumour suppressor genes reveal clues about how cetaceans resist cancer

Cetaceans are the longest-lived mammals and cancer-resistant species. They have developed mechanisms against cancer, although the underlying molecular bases of these remain unknown. We investigated the role of natural selection in the evolution of 1077 tumour suppressor genes (TSGs) in cetaceans. We found a signal of positive selection in important regulators of DNA-damage, tumour dissemination, and immune system. The turnover rate was almost 2.4-fold higher in cetaceans as compared to other mammals. Additionally, we report 71 genes with duplications, of which 11 genes are linked to longevity. This study provides novel insights into the genetic basis of disease resistance.

Cancer resisting cetacean - Cetaceans - whales, dolphins and porpoises - are the longest-lived mammals and cancer-resistant species. This study found cetaceans gained and lost genes related to tumor suppression at a rate 2.4 times higher than other mammals, with signs of positive genetic selection in genes regulating DNA-damage, tumour dissemination, and the immune system. It also identified duplication of 11 genes linked to longevity.

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Journal/
conference: Proceedings of the Royal Society B

Research:Paper

Organisation/s: Universidad Austral de Chile, Chile

Funder: Comisión Nacional de Investigación Científica y Tecnológica (CONICYT)—Chile through the doctoral scholarship no. 21170433 and the scholarship from MECESUP AUS2003 to D.T.-M. Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT) grant no. 1160627 and Millennium Nucleus of Ion Channels Associated Diseases (MiNICAD), Iniciativa Científica Milenio, Ministry of Economy, Development and Tourism, Chile, to J.C.O. AnAge is supported by funding from the Biotechnology and Biological Sciences Research Council (BB/R014949/1) to J.P.d.M.

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