Devil Facial Tumour Disease (DFTD) is a contagious cancer that is spread between Tasmanian devils when they bite each other. The cancer was first seen in 1996 and is believed to have been derived from a Schwann cell or Schwann cell-like precursor. The cancer is clonal and karyotypic strains have been observed. The cancer has killed 85% of devils and threatens the species with extinction in the wild.

In this talk I will focus on two aspects of DFTD evolution: telomeres and methylation. We have shown that DFTD cells have short telomeres and that telomere copy number does not differ between DFTD strains. Telomere copy number has increased over time. DFTD appears to have evolved to monitor and regulate the length of telomeres: shorter telomeres become elongated by up-regulation of telomerase-related genes and longer telomeres are protected from further elongation by members of the shelterin complex. We believe this mechanism explains the lack of spatial and strain specific patterns in telomere copy number.

Preliminary work on the DFTD epigenome does not reveal any strain or region specific epimutations. However, we have observed a significant increase in hypomethylation of DFTD over time. This does not appear to be the result of a maintenance deficiency as the DNA methytransferase-1 gene is up-regulated. Instead, active demethylation appears to be occurring, supported by the temporal increase in MBD2 and MBD4.

Taken together, our findings are pointing towards DFTD being an evolving parasite. Understanding the evolutionary trajectory of this cancer will be important for management of the species in the wild. The disease also provides a unique opportunity to study cancer evolution and progression in a model where the cancer does not die with its host.