Transmission of devil facial-tumour disease

Pearse, Anne-Maree; Swift, Kate

doi:10.1038/439549a

Cited by 412 publications

(464 citation statements)

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“…Infectious cancers have been demonstrated in only two mammal species so far, a group for which cancer is much more studied than in others. A sexually transmitted venereal tumor was reported in dogs (Murgia, Pritchard, Kim, Fassati, & Weiss, 2006) while malignant cells of facial tumors were identified to be transmitted by biting in Tasmanian devils (Pearse & Swift, 2006). Two key elements of transmissible cancer emergence are the survival of malignant cells during transmission from host to host and the resistance to immune attacks in the new host (Ujvari, Gatenby, & Thomas, 2016).…”

Section: Transmissible Cancers Might Be More Widespread Than Previousmentioning

confidence: 99%

Weird genotypes? Don't discard them, transmissible cancer could be an explanation

Riquet

Simon

Bierne

2016

Evolutionary Applications

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Genetic chimerism is rarely considered in the analysis of population genetics data, because assumed to be an exceptionally rare, mostly benign, developmental accident. An unappreciated source of chimerism is transmissible cancer, when malignant cells have become independent parasites and can infect other individuals. Parasitic cancers were thought to be rare exceptions, only reported in dogs (Murgia et al., Cell, 2006, 126, 477; Rebbeck et al., Evolution, 2009, 63, 2340), Tasmanian devils (Pearse and Swift, Nature, 2006, 439, 549; Pye et al., Proceedings of the National Academy of Sciences, 2016, 113, 374), and soft‐shell clams (Metzger et al., Cell, 2015, 161, 255). However, the recent simultaneous report of four new contagious leukemias in marine mollusks (Metzger et al., Nature, 2016, 534, 705) might change the rules. By doubling up the number of naturally occurring transmissible cancers, this discovery suggests they may essentially be missed because not sufficiently searched for, especially outside mammals. We encourage population geneticists to keep in mind infectious cancer when interpreting weird genotypes in their molecular data. It would then contribute in the investigation of how widespread contagious cancer could really be in the wild. We provide an example with our own data in Mytilus mussels, a commercially important shellfish. We identified genetic chimerism in a few mussels that suggests the possible occurrence at low prevalence in European M. edulis populations of a M. trossulus contagious cancer related to the one described by Metzger et al. (Nature, 2016, 534, 705) in populations of British Columbia.

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Section: Transmissible Cancers Might Be More Widespread Than Previousmentioning

confidence: 99%

Weird genotypes? Don't discard them, transmissible cancer could be an explanation

Riquet

Simon

Bierne

2016

Evolutionary Applications

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“…DFTD arose in a Tasmanian devil in northeastern Tasmania but has since spread to all devil populations in eastern and central Tasmania (1,22). DFTD cells are thought to pass between animals when they bite each other during social interactions and, once transmitted, large tumors form around the face and neck that cause 100% mortality (1).…”

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confidence: 99%

“…The emergence of DFTD triggered immediate comparisons to the only other naturally occurring contagious cancer, canine transmissible venereal tumor (CTVT) (1,2). CTVT is a sexually transmitted tumor in dogs that has existed as a parasitic cell line for thousands of years (2,3).…”

mentioning

confidence: 99%

“…However, contagious cancers can emerge in nature and provide a unique opportunity to study mechanisms of immune escape and tumor evolution in cancers that are continually passaged between individuals. Devil facial tumor disease (DFTD) is one such contagious cancer that emerged 16 y ago in the Tasmanian devil, a marsupial carnivore found only on the island of Tasmania (1).…”

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confidence: 99%

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Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer

Siddle

Kreiss

Tovar

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

200

306

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Contagious cancers that pass between individuals as an infectious cell line are highly unusual pathogens. Devil facial tumor disease (DFTD) is one such contagious cancer that emerged 16 y ago and is driving the Tasmanian devil to extinction. As both a pathogen and an allograft, DFTD cells should be rejected by the host-immune response, yet DFTD causes 100% mortality among infected devils with no apparent rejection of tumor cells. Why DFTD cells are not rejected has been a question of considerable confusion. Here, we show that DFTD cells do not express cell surface MHC molecules in vitro or in vivo, due to down-regulation of genes essential to the antigen-processing pathway, such as β 2 -microglobulin and transporters associated with antigen processing. Loss of gene expression is not due to structural mutations, but to regulatory changes including epigenetic deacetylation of histones. Consequently, MHC class I molecules can be restored to the surface of DFTD cells in vitro by using recombinant devil IFN-γ, which is associated with up-regulation of the MHC class II transactivator, a key transcription factor with deacetylase activity. Further, expression of MHC class I molecules by DFTD cells can occur in vivo during lymphocyte infiltration. These results explain why T cells do not target DFTD cells. We propose that MHC-positive or epigenetically modified DFTD cells may provide a vaccine to DFTD. In addition, we suggest that down-regulation of MHC molecules using regulatory mechanisms allows evolvability of transmissible cancers and could affect the evolutionary trajectory of DFTD.

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“…Transmissible cancers have also been referred to in speciation terms. Three come to mind: Canine transmissible venereal tumor (CTVT, [Murgia et al, 2006;Rebbeck et al, 2009]); the facial cancer of the Tasmanian Devil (Sarcophilus harrisii, a marsupial [Nowak, 1999;Dingliore and Nowak, 2006;Pearse and Swift, 2006]); and the transmissible cancer of Syrian hamsters [Copper et al, 1964].…”

Section: Appendix: Cancer An Atavism?mentioning

confidence: 99%

Annals of morphology. Atavisms: Phylogenetic lazarus?

Zanni

Opitz

2013

American J of Med Genetics Pt A

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Dedication: with highest respect and affection to Prof. Giovanni Neri on the eve of his official administrative retirement as Chair of the Institute of Medical Genetics of the Università Cattolica of Rome for leadership in medical genetics and medical science and friendship for decades. The concept “atavism,” reversion, throwback, Rückschlag remains an epistemological challenge in biology; unwise or implausible over‐interpretation of a given structure as such has led some to almost total skepticism as to its existence. Originating in botany in the 18th century it became applied to zoology (and humans) with increasing frequency over the last two centuries such that the very concept became widely discredited. Presently, atavisms have acquired a new life and reconsideration given certain reasonable criteria, including: Homology of structure of the postulated atavism to that of ancestral fossils or collateral species with plausible soft tissue reconstructions taking into account relationships of parts, obvious sites of origin and insertion of muscles, vascular channels, etc. Most parsimonious, plausible phylogenetic assumptions. Evident rudimentary or vestigial anatomical state in prior generations or in morphogenesis of a given organism. Developmental instability in prior generations, that is, some closely related species facultatively with or without the trait. Genetic identity or phylogenomic similarity inferred in ancestors and corroborated in more or less closely related species. Fluctuating asymmetry may be the basis for the striking evolutionary diversification and common atavisms in limbs; however, strong selection and developmental constraints would make atavisms in, for example, cardiac or CNS development less likely.Thus, purported atavisms must be examined critically in light of the above criteria. © 2013 Wiley Periodicals, Inc.

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Transmission of devil facial-tumour disease

Cited by 412 publications

References 8 publications

Weird genotypes? Don't discard them, transmissible cancer could be an explanation

Weird genotypes? Don't discard them, transmissible cancer could be an explanation

Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer

Annals of morphology. Atavisms: Phylogenetic lazarus?

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