Cancers aren’t usually contagious, but a tiny number of them can spread when diseased cells move from one animal to another. One such cancer, an aggressive facial tumor, has wiped out large numbers of Tasmanian devils in Australia over the past two decades. Now, scientists have reported a second contagious facial cancer in these endangered marsupials.
The original Tasmanian devil facial tumor disease (DFTD), discovered in 1996, causes cancerous masses on the head and inside the mouth, and is thought to spread when the ferocious animals bite each other. Only two other contagious cancers have been found in nature—one in dogs and one in soft-shelled clams—leading researchers to propose that such conditions represent extremely rare events. Finding a second transmissible cancer in Tasmanian devils came as a shock, says study co-senior author Gregory Woods, an immunologist at the University of Tasmania.
“For it to happen twice in one species just seemed too incredible to be true,” says Woods. “It suggests that transmissible cancers may be more common than we first thought.” The team reported its discovery and analysis of the new cancer, called DFT2, in the Jan 12 issue of PNAS.
On the surface, the two Tasmanian devil cancers appear indistinguishable. Woods’s team collected the initial DFT2 sample from an animal with suspected DFTD (which they later re-named DFT1). But when researchers examined the tissue under a microscope, they found cancer cells that grew in sheet-like configurations, instead of the characteristic cell bundles formed by DFT1. At first, Woods says he chalked up the anomaly to a spontaneous cancer in a single animal. Months later, a second case appeared with the same unusual cell-growth pattern.
Suspecting that they had stumbled across a new line of contagious cancer cells, the group ran genetic tests on the two samples and other Tasmanian devil tumors they had collected. Eventually, they reported five cases that shared identical chromosomal abnormalities, which were clearly different from those observed in DFT1. Whereas DFT1 arose in a female host, these samples contained both an X and a Y chromosome, suggesting that the second cancer had originated and spread from a male devil.
“It looks as if it’s a completely separate derivation,” says virologist Robin Weiss, who has studied contagious cancer in dogs at University College London. “It raises questions about why this should happen a second time, and whether there’s something special about those devils.”
A combination of factors may make the Tasmanian devils particularly susceptible, the authors suggest. Their tendency to bite each other a lot, especially on the face, helps to transfer cancer cells that grow on the face and in the mouth. Furthermore, Tasmanian devil populations have low genetic diversity—a likely consequence of declining numbers and inbreeding. This effect could prevent the animals’ immune systems from recognizing and rejecting foreign cells as readily.
“We need to be alert,” says Woods, who warns that vigilance is needed to protect ‘insurance populations’ of healthy Tasmanian devils that are being bred to help boost the wild populations. Woods is now interested in monitoring the spread of DFT2, and understanding precisely how the cancer evades the immune system. His team is currently conducting vaccine research to combat DFT1, which they hope also to extend to DFT2.