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Transmissible cancers are infectious malignant cell clones that spread among individuals through transfer of living cancer cells. Several such clones have been identified in various species of marine bivalve molluscs, including mussels, clams and cockles. These parasitic cell lineages cause a leukaemia‐like disease called disseminated neoplasia, and are presumed to pass between hosts by ingestion of water‐borne cancer cells during filter feeding. Although occasional cases of transmissible cancer had previously been identified in mussels of the genus Mytilus in Europe, the number of distinct clones affecting these animals, and their prevalence, was unknown. In this issue of Molecular Ecology, Hammel et al. (2021) present findings from a large‐scale screen for transmissible cancer across 5907 European Mytilus mussels. Using a genotyping approach, Hammel et al. searched for signal of genetic chimerism, which can arise due to infection by transmissible cancer cells. The screen detected a previously identified globally distributed mussel transmissible cancer at very low prevalence, and found no evidence of additional contagious clones. A parallel histological screen additionally revealed low prevalence of a nontransmissible form of disseminated neoplasia. By quantifying the burden of disseminated neoplasia in European mussel populations, this study provides strong foundations for future work investigating the origins, evolution and impacts of transmissible cancers in mussels. [ABSTRACT FROM AUTHOR]

Devil facial tumour disease (DFTD) comprises two genetically distinct transmissible cancers (DFT1 and DFT2) endangering the survival of the Tasmanian devil (Sarcophilus harrisii) in the wild. DFT1 first arose from a cell of the Schwann cell lineage; however, the tissue-of-origin of the recently discovered DFT2 cancer is unknown. In this study, we compared the transcriptome and proteome of DFT2 tumours to DFT1 and normal Tasmanian devil tissues to determine the tissue-of-origin of the DFT2 cancer. Our findings demonstrate that DFT2 expresses a range of Schwann cell markers and exhibits expression patterns consistent with a similar origin to the DFT1 cancer. Furthermore, DFT2 cells express genes associated with the repair response to peripheral nerve damage. These findings suggest that devils may be predisposed to transmissible cancers of Schwann cell origin. The combined effect of factors such as frequent nerve damage from biting, Schwann cell plasticity and low genetic diversity may allow these cancers to develop on rare occasions. The emergence of two independent transmissible cancers from the same tissue in the Tasmanian devil presents an unprecedented opportunity to gain insight into cancer development, evolution and immune evasion in mammalian species. [ABSTRACT FROM AUTHOR]

Background: The canine transmissible venereal tumour (CTVT) is a contagious cancer spread by the direct transfer of living cancer cells. CTVT usually spreads during mating, manifesting as genital tumours. However, oronasal CTVT is also occasionally observed, and presumably arises through oronasal contact with genital CTVT tumours during sniffing and licking. Methods: Given that sniffing and licking transmission behaviours may differ between sexes, we investigated whether oronasal CTVT shows sex disparity. Results: Twenty‐seven of 32 (84%) primary oronasal tumours in a CTVT tumour database occurred in males. In addition, 53 of 65 (82%) primary oronasal CTVT tumours reported in the published literature involved male hosts. These findings suggest that male dogs are at four to five times greater risk of developing primary oronasal CTVT than females. This disparity may be due to sex differences in licking and sniffing activity, perhaps also influenced by sex differences in CTVT accessibility for these behaviours. Conclusion: Although oronasal CTVT is rare, it should be considered as a possible diagnosis for oronasal tumours, particularly in male dogs. [ABSTRACT FROM AUTHOR]

Summary: The Tasmanian devil (Sarcophilus harrisii), the largest marsupial carnivore, is endangered due to a transmissible facial cancer spread by direct transfer of living cancer cells through biting. Here we describe the sequencing, assembly, and annotation of the Tasmanian devil genome and whole-genome sequences for two geographically distant subclones of the cancer. Genomic analysis suggests that the cancer first arose from a female Tasmanian devil and that the clone has subsequently genetically diverged during its spread across Tasmania. The devil cancer genome contains more than 17,000 somatic base substitution mutations and bears the imprint of a distinct mutational process. Genotyping of somatic mutations in 104 geographically and temporally distributed Tasmanian devil tumors reveals the pattern of evolution and spread of this parasitic clonal lineage, with evidence of a selective sweep in one geographical area and persistence of parallel lineages in other populations. PaperClip: Display Omitted [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]