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Nat Commun. 2016 Aug 30;7:12684. doi: 10.1038/ncomms12684.

Rapid evolutionary response to a transmissible cancer in Tasmanian devils.

Author information

1
School of Biological Sciences, Washington State University, Pullman, Washington 99164-4236, USA.
2
School of Zoology, University of Tasmania, Private Bag 5, Hobart, Tasmania 7001, Australia.
3
Department of Biological Sciences, Institute for Bioinformatics and Evolutionary Studies, University of Idaho, 875 Perimeter Drive, Moscow, Idaho 83844-3051, USA.
4
School of Environment, Griffith University, Nathan Campus, 170 Kessels Road, Nathan, Queensland 4111, Australia.
5
Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.

Abstract

Although cancer rarely acts as an infectious disease, a recently emerged transmissible cancer in Tasmanian devils (Sarcophilus harrisii) is virtually 100% fatal. Devil facial tumour disease (DFTD) has swept across nearly the entire species' range, resulting in localized declines exceeding 90% and an overall species decline of more than 80% in less than 20 years. Despite epidemiological models that predict extinction, populations in long-diseased sites persist. Here we report rare genomic evidence of a rapid, parallel evolutionary response to strong selection imposed by a wildlife disease. We identify two genomic regions that contain genes related to immune function or cancer risk in humans that exhibit concordant signatures of selection across three populations. DFTD spreads between hosts by suppressing and evading the immune system, and our results suggest that hosts are evolving immune-modulated resistance that could aid in species persistence in the face of this devastating disease.

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