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More than 10,000 years ago, before the first dog was even domesticated, a canine cancer formed in a single wolf or East Asian dog and began passing like a parasite to other similar animals.
Sexually transmitted, this incredibly successful clonal cancer has survived through the millennia and is seen in dogs around the world today.
The canine transmissible venereal tumour, or CTVT, holds valuable secrets that researchers are hoping to unlock. Ongoing studies could shed light on human diseases as well as the deadly contagious cancer ravaging the Tasmanian devil in Australia.
At Britain's Wellcome Sanger Trust Institute, Elizabeth Murchison is sequencing the genome of several samples of CTVT that are among hundreds she has collected from around the world. The disease is most commonly found in feral or pack animals. Murchison's samples come from places where dogs wander freely in Mexico, parts of South America and Asia.
CTVT spreads when dogs mate, or bite, lick or sniff a tumour. Unlike other cancers, the chromosomes of CTVT cells are distinct, so that the tumour cells on any two dogs are more closely related to each other than they are to the dogs.
"It's pretty remarkable that a single cell line has survived all this time," says Murchison. "It's the oldest remaining derived life form that's continuously living that we know of by far. And it's the only thing we know of that's spread around the world as a clone."
One reason it's been able to survive for so long is that it doesn't kill its hosts. The cancer rarely metastasises and within six months or so it regresses. It's also highly responsive to chemotherapy.
What's more, CTVT seems to have created a fountain of youth for itself. Researchers from Imperial College London reported in Science last year that the tumour periodically replenishes its energy supply by stealing a new host's healthy mitochondria. Mitochondria are a cell's fuel generators.
The scientists speculated that the tumour's own mitochondria are weakened by mutations over generations. By stealing new resources the tumour can grow more quickly. "It's an important evolutionary advancement of the cancer that it's able to prevent its own degeneration by stealing the necessary requirements from a cell that doesn't have this problem," says Clare Rebbeck, a former researcher from the team who's now at the Cold Spring Harbour Laboratory in New York. "It seems like a first in evolution."
The mitochondria findings could have implications on cell therapies for human diseases, such as strokes and heart attacks that are characterised by ischemia and reperfusion followed by a failure of mitochondria.
With the sequencing of the CTVT genome expected to wrap up later this year, Murchison hopes it will not only produce further information about how the cancer emerged and diverged as it spread around the world, but it could also enhance human immunological research. "If we could understand how these tumours evade immune detection, that could give us insight into how the immune system works in detecting grafts, and perhaps could lead to applications that could help patients who receive organ transplants," says Murchison.
