Clonally transmissible cancers in dogs and Tasmanian devils

Murchison, Elizabeth P.

doi:10.1038/onc.2009.350

Cited by 143 publications

(163 citation statements)

References 90 publications

(180 reference statements)

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“…The devil transmissible tumour is spread by biting [19], resulting in tumours inside and around the mouth, and is almost always fatal 6-12 months from the appearance of clinical signs [20]. Both DFTD and CTVT have evolved mechanisms of immune escape in allogeneic hosts, in part via epigenetic downregulation of major histocompatibility complex (MHC) gene expression in tumour cells [14,21].…”

Section: Introductionmentioning

confidence: 99%

“…Directly transmissible cancers, in which the pathogen is a clonal infectious cell line spread through injurious contact [14], are particularly rare in nature. They are known only in the recently emerged Tasmanian devil facial tumour disease (DFTD) [15], which threatens its unique host, the Tasmanian devil (Sarcophilus harrisii), with extinction [16], a leukaemia-type disease affecting soft-shell clams in North America [17], and the much older (approx.…”

Section: Introductionmentioning

confidence: 99%

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Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response

et al. 2015

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Tasmanian devil facial tumour disease (DFTD) is a clonally transmissible cancer threatening the Tasmanian devil (Sarcophilus harrisii) with extinction. Live cancer cells are the infectious agent, transmitted to new hosts when individuals bite each other. Over the 18 years since DFTD was first observed, distinct genetic and karyotypic sublineages have evolved. In this longitudinal study, we investigate the associations between tumour karyotype, epidemic patterns and host demographic response to the disease. Reduced host population effects and low DFTD infection rates were associated with high prevalence of tetraploid tumours. Subsequent replacement by a diploid variant of DFTD coincided with a rapid increase in disease prevalence, population decline and reduced mean age of the population. Our results suggest a role for tumour genetics in DFTD transmission dynamics and epidemic outcome. Future research, for this and other highly pathogenic emerging infectious diseases, should focus on understanding the evolution of host and pathogen genotypes, their effects on susceptibility and tolerance to infection, and their implications for designing novel genetic management strategies. This study provides evidence for a rapid localized lineage replacement occurring within a transmissible cancer epidemic and highlights the possibility that distinct DFTD genetic lineages may harbour traits that influence pathogen fitness.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response

et al. 2015

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“…The re-introduction of grey wolves into Yellowstone Park in North America 100 years after they were extirpated, resulted in both behavioural and density changes of herbivore populations, leading to reduced grazing pressure [42]. The expected outcome of the facial tumour epidemic in devils based on other host/pathogen interactions is evolution of reduced pathogen virulence leading to coexistence [47], a course followed by the only other naturally occurring transmissible cancer, Canine Transmissible Venereal Sarcoma [48]. Evolution of DFTD to an endemic disease that allows persistence or recovery of the devil is likely to take decades, a timescale on which evolutionary change in prey populations could occur.…”

Section: Discussionmentioning

confidence: 99%

Relaxation of risk-sensitive behaviour of prey following disease-induced decline of an apex predator, the Tasmanian devil

et al. 2015

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Apex predators structure ecosystems through lethal and non-lethal interactions with prey, and their global decline is causing loss of ecological function. Behavioural changes of prey are some of the most rapid responses to predator decline and may act as an early indicator of cascading effects. The Tasmanian devil ( Sarcophilus harrisii ), an apex predator, is undergoing progressive and extensive population decline, of more than 90% in long-diseased areas, caused by a novel disease. Time since local disease outbreak correlates with devil population declines and thus predation risk. We used hair traps and giving-up densities (GUDs) in food patches to test whether a major prey species of devils, the arboreal common brushtail possum ( Trichosurus vulpecula ), is responsive to the changing risk of predation when they forage on the ground. Possums spend more time on the ground, discover food patches faster and forage more to a lower GUD with increasing years since disease outbreak and greater devil population decline. Loss of top–down effects of devils with respect to predation risk was evident at 90% devil population decline, with possum behaviour indistinguishable from a devil-free island. Alternative predators may help to maintain risk-sensitive anti-predator behaviours in possums while devil populations remain low.

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“…In Tasmanian devil facial tumour disease (TDFD) and canine transmissible venereal tumour (CTVT), the infecting agent of the cancer is known to be the cancer cell itself [129]. TDFD results from cancer cells that are transmitted among Tasmanian devils (Sarcophilus harrisii) by biting during aggressive interactions; CTVT is similarly transmitted among dogs by licking and biting [129].…”

Section: Transmissible Cancer Cellsmentioning

confidence: 99%

Infection and cancer in multicellular organisms

Ewald

2015

Phil. Trans. R. Soc. B

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Evolutionary considerations suggest that oncogenic infections should be pervasive among animal species. Infection-associated cancers are well documented in humans and domestic animals, less commonly reported in undomesticated captive animals, and rarely documented in nature. In this paper, we review the literature associating infectious agents with cancer to evaluate the reasons for this pattern. Non-malignant infectious neoplasms occur pervasively in multicellular life, but oncogenic progression to malignancy is often uncertain. Evidence from humans and domestic animals shows that non-malignant infectious neoplasms can develop into cancer, although generally with low frequency. Malignant neoplasms could be difficult to find in nature because of a low frequency of oncogenic transformation, short survival after malignancy and reduced survival prior to malignancy. Moreover, the evaluation of malignancy can be ambiguous in nature, because criteria for malignancy may be difficult to apply consistently across species. The information available in the literature therefore does not allow for a definitive assessment of the pervasiveness of infectious cancers in nature, but the presence of infectious neoplasias and knowledge about the progression of benign neoplasias to cancer is consistent with a widespread but largely undetected occurrence.

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Clonally transmissible cancers in dogs and Tasmanian devils

Cited by 143 publications

References 90 publications

Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response

Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response

Relaxation of risk-sensitive behaviour of prey following disease-induced decline of an apex predator, the Tasmanian devil

Infection and cancer in multicellular organisms

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