Transmissible cancers are fascinating biological entities, only recently discovered. They have acquired the ability to cross host boundaries to spread between animals, even sometimes interspecifically, by the direct transfer of cancerous cells. They have been shown to persist for hundreds or thousands of years in host populations. A puzzling issue is that, in the absence of known sexual-like reproduction mechanisms, transmissible cancers must cope with clonal degeneration that could limit their persistence. Several transmissible cancer lineages have been described in Bivalvia, all of them displaying hyperploidy. Some sub-lineages (i.e. descending from a common founder host) with distinct degrees of hyperploidy (2 to 10 times the host cell content) coexist in mussel populations. Hence, the hypothesis that hyperploidization concurs to the persistence and long-term evolution of these transmissible cancers is appealing to consider. HYPERCAN aims to decipher how hyperploidy, in mussel transmissible cancers (MtrBTN) that evolve for hundreds of years, influence the cancer fitness and contribute to facing the clonal degeneration and to generating sufficient genetic diversity to persist in host populations in absence of sexual reproduction.




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