Characteristics
Tasmanian devil cells have 14 chromosomes, while the oldest-known strain of the tumor cell contains thirteen chromosomes, nine of which are recognizable and four of which are mutated “marker” chromosomes. More recently-evolved strains have an additional mutant marker chromosome, for a total of fourteen chromosomes. Researchers identified the cancer as a neuroendocrine tumor, and found identical chromosomal rearrangements in all the cancer cells. The karyotype anomalies of DFTD cells are similar to those of cancer cells from canine transmissible venereal tumour (CTVT), a cancer of dogs that is transmitted between canines by physical contact.
The theory that cancer cells themselves could be an infective agent (the Allograft Theory) was first supported by the researchers A-M. Pearse, K. Swift, and colleagues. In 2006, Pearse and Swift analyzed DFTD cells from several devils in different locations, and determined that all of the DFTD cells were not only genetically identical to each other, but also genetically distinct from their hosts, and from all known Tasmanian devils. Thus, the cancer must have originated in a single individual and spread, rather than arising separately within each individual. Later researchers witnessed a previously-uninfected devil develop tumors from lesions caused by an infected devil’s bites, confirming that the disease is spread by allograft, and that the normal methods of transmission include biting, scratching, and aggressive sexual activity between individuals. Since June 2005, three females have been found that are partially resistant to DFTD.
Further research from the University of Sydney has shown that the infectious facial cancer may be able to spread because of low diversity in devil immune genes (MHC class I and II). The same genes are also found in the tumors, so the devil's immune system does not recognise the tumor cells as foreign. There are at least four, and most likely more, strains of the cancer, showing that it is evolving, and may become more virulent. The strains may also complicate attempts to develop a vaccine, and the mutation of the cancer may mean that it could spread to other related species, like the quoll.
In a paper published in the January 2010 issue of Science, an international team of researchers announced that devil facial tumor disease likely originated in the Schwann cells, of a single devil, most likely a female. Schwann cells are found in the peripheral nervous system, and produce myelin and other proteins essential for the functions of nerve cells in the peripheral nervous system. The researchers sampled 25 tumors and found that the tumors were genetically identical. Using deep sequencing technology, they then profiled the tumors' transcriptome, the set of genes that are active in tumors. The transcriptomes closely matched those of Schwann cells, revealing high activity in many of the genes coding for myelin basic protein production. Several specific markers were identified by the team, including the MBP and PRX genes, which may enable veterinarians to more easily distinguish DFTD from other types of cancer, and may eventually help identify a genetic pathway that can be targeted to treat it.
Due to the decreased life expectancy of the devils due to DFTD, they have begun breeding at younger ages in the wild, with reports that many only live to participate in one breeding cycle. A study has suggested that Tasmanian devils have changed their breeding habits in response to the disease. Females previously started breeding at the age of two, then annually for about three more years until dying normally. Now they commonly breed at the age of one, and die of tumours shortly thereafter. It is speculated that the disease is spread by devils biting each other during the mating season. Social interactions have been seen spreading DFTD in a local area. It is one of three known contagious cancers.
Read more about this topic: Devil Facial Tumour Disease