Inter-individual transmission of cancer cells represents an intriguing and unexplored host-pathogen system, with significant ecological and evolutionary ramifications. The pathogen consists of clonal malignant cell lines that spread horizontally as allografts and/or xenografts. Although only nine transmissible cancer lineages in eight host species from both terrestrial and marine environments have been investigated, they exhibit evolutionary dynamics that may provide novel insights into tumor-host interactions particularly in the formation of metastases. Here we present an overview of known transmissible cancers, discuss the necessary and sufficient conditions for cancer transmission, and provide a comprehensive review on the evolutionary dynamics between transmissible cancers and their hosts.

Transmissible cancers are elusive and understudied parasitic life forms caused by malignant clonal cells (nine lineages are known so far). They emerge by completing sequential steps that include breaking cell cooperation, evade anti‐cancer defences and shedding cells to infect new hosts. Transmissible cancers impair host fitness, and their importance as selective force is likely largely underestimated. It is, therefore, crucial to determine how common they might be in the wild. Here, we draw a parallel between the steps required for a transmissible cancer to emerge and the steps required for an intelligent civilisation to emerge in the Milky Way using a modified Drake equation. Using numerical analyses, we estimate the potential number of extant marine and bivalve species in which transmissible cancers might exist. Our results suggest that transmissible cancers are more common than expected, and that new lineages can be found by screening a large number of species.

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Strong and ongoing artificial selection in domestic animals has resulted in amazing phenotypic responses that benefit humans, but often at a cost to an animal's health, and problems related to inbreeding depression, including a higher incidence of cancer. Despite high rates of cancer in domesticated species, little attention has been devoted to exploring the hypothesis that persistent artificial selection may also favour the evolution of compensatory anticancer defences. Indeed, there is evidence for effective anti‐cancer defences found in several domesticated species associated with different cancer types. We also suggest that artificial selection can favour the “domestication” of inherited oncogenic mutations in rare instances, retaining those associated to late and/or less aggressive cancers, and that by studying these seemingly rare anticancer adaptations, novel cancer treatments may be found.