![]() We suggest a scenario in which transmissible malignant allografts engage in an evolutionary tug-of-war with their host similar to that observed in host–parasite interactions. We propose and discuss several key factors that are necessary for malignant cell transmission and successful establishment in the novel host environment, such as the ability to bypass/downregulate histocompatibility barriers, propagule number, phenotypic plasticity, as well as permissive host environment. Here we review the biology of transmissible cancers observed under laboratory conditions and in the wild and discuss the evolutionary and ecological impact of the latter. So far only three transmissible cancers have been identified. To facilitate a description of devil facial tumor disease, this review uses life cycles of parasites as an analogy.Īlthough transmissible cancers have been documented under laboratory conditions, naturally occurring transmissible contagious cancers with no underlying pathogen infections are rare in the wild. However, unlike many parasites, the DFTD cancer cells have a simple lifecycle and do not have either independent, vector-borne, or quiescent phases. Through direct contact between devils, DFTD has spread throughout the devil population. Devil facial tumor disease is a transmissible cancer and, therefore, DFTD shares one additional feature common to most parasites. The Centers for Disease Control and Prevention (CDC) defines a parasite as “An organism that lives on or in a host organism and gets its food from, or at, the expense of its host.” Most cancers, including DFTD, live within a host organism and derive resources from its host, and consequently have parasitic-like features. The cancer cells are derived from Schwann cells and are spread between devils during biting, a common behavior during the mating season. Understanding the role of epimutations in the evolution of this parasitic cancer will provide unique insights into the role of epigenetic plasticity in cancer evolution and progression in traditional cancers that arise and die with their hosts.ĭevil facial tumor disease (DFTD) encompasses two independent transmissible cancers that have killed the majority of Tasmanian devils. Our work shows that DFTD should not be treated as a static entity, but rather as an evolving parasite with epigenetic plasticity. The implications of these changes on disease phenotypes need to be explored. Instead, we believe that loss of methylation is owing to active demethylation, supported by the temporal increase in MBD2 and MBD4 (p < 0.001). We propose that loss of methylation is not because of a maintenance deficiency, as an upregulation of DNA methyltransferase 1 gene was observed in tumours compared with nerves (p < 0.005). However, we revealed a significant increase in hypomethylation in DFT samples over time (p < 0.0001). ![]() We did not observe any strain or region-specific epimutations. We show that tumour cells have similar levels of methylation to peripheral nerves, the tissue from which DFTD originated. In the present study, we explore the Devil Facial Tumour (DFT) epigenome and the genes involved in DNA methylation homeostasis. The cancer is a genetically and chromosomally stable clonal cell line which is transmitted by biting during social interactions. The emergence of Devil Facial Tumour Disease (DFTD), a highly contagious cancer, is driving Tasmanian devils (Sarcophilus harrisii) to extinction. ![]()
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