Twenty years ago, scientists identified a bizarre new disease afflicting Australia’s Tasmanian devils. These black, rambunctious, corgi-sized predators started turning up with grotesque facial tumors that proved invariably fatal. The disease, aptly named devil facial tumor disease (DFTD), quickly spread through the devils’ island home of Tasmania, slashing their numbers by up to 90 percent in some regions, and consigning them to the endangered-species list in 2008.
After a decade, scientists realized that all cases of DFTD are genetically identical. The tumors were all clones of each other, and distinct from the devils that harbor them. The conclusion was clear and astonishing—DFTD is a contagious cancer, and the devils were catching it from each other.
Cancers are almost always confined to a single body: when their host dies, so do they. But in the Tasmanian devils, one particular tumor had evolved the ability to jump from host to host. The boisterous devils spread this transmissible tumor when they squabble over carcasses and bite each other in the face.
Contagious cancers don’t exist in humans; we can develop cancer after contracting infections like the HPV virus or the bacterium Helicobacter pylori, but the tumors themselves can’t spread between people. In fact, DFTD is one of only three known wild transmissible tumors. There’s also CTVT, a venereal tumor of dogs, which arose around 11,000 years ago, and has since conquered the world by hitchhiking on the genitals of domestic pooches. And there’s a water-borne leukemia that’s spreading through North America’s soft-shell clams. That’s it.
“They’re flukes of nature,” says Elizabeth Murchison from the University of Cambridge, who has studied DFTD for years. “Our whole paradigm about transmissible cancers is that they’re extraordinarily rare.”
Or are they?
In March 2014, Murchison’s colleague Ruth Pye, a graduate student at the University of Tasmania, noticed something weird about a facial tumor taken from a devil captured just north of Hobart. Physically, it looked like DFTD; genetically, it was clearly something different. For example, DFTD cells have lost their X and Y sex chromosomes, both of which were present in the new tumor. Pye reasoned that this particular devil had spontaneously developed its own type of facial tumor that looked like DFTD, but wasn’t. It was a one-off.
Except, a few months later, she found the same genetically distinct tumor in a second devil from the same area. In both cases, the tumors bore absolutely no genetic resemblance to either DFTD or their respective hosts. These devils had developed a second type of contagious cancer.
“We absolutely couldn’t believe it,” says Murchison. “It’s the last thing I could have possibly imagined.”
The team has now found the new tumor in eight devils, all from the same southeastern corner of Tasmania. They call it DFT2, and they’ve relabelled the original as DFT1. Both cause similar symptoms, but their cells are different enough that a trained vet can easily tell them apart down a microscope. They seem to have originated from different tissues, and as Pye observed, they are genetically very different.
To develop one transmissible tumor may be regarded as a misfortune; to develop two looks like carelessness. “It’s telling us that there’s something we don’t understand about these cancers,” says Murchison. “They’ve arisen twice in Tasmanian devils in the last 30 years, which suggests that maybe they’re not that rare.”
It could be that the devils are extraordinarily susceptible to these kinds of cancers. A historical population crash left them with very low genetic diversity, which perhaps stops their immune systems from recognizing the foreign cancer cells and fighting them off. They also bite each other on the face a lot, which provides an easy route of transmission.
But that doesn’t explain why DFT1 and DFT2 didn’t exist before the 1990s. It’s unlikely that scientists simply didn’t notice; as Murchison says, you can’t miss tumors that are that obvious. “Maybe something is triggering them, some kind of predisposing agent or infection,” says Murchison. “We really don’t understand it.”
There’s a chance that DFT2 isn’t entirely new. It could have arisen when a DFT1 cell fused with a healthy one, picking up some new genetic material along the way. There’s no evidence to suggest that this happened, but the team can’t rule out the possibility yet.
It matters, because the rise of a second contagious cancer has important implications for the future of the devils. Researchers have been trying to capture and store healthy individuals in “insurance populations” that are protected from DFTD. “But if the disease can spontaneously arise, it might mean that devils aren’t safe, even in an captive or insurance population,” says Murchison. “There’s a lot of discussion here in Tasmania about what the implications are and what we now need to do.”
There’s one silver lining: DFT2 could help scientists to better understand DFT1, its more common and problematic cousin. “Any mutations that are common to both of them are probably going to be important,” says Murchison. “I’m hoping it’s a chance to learn more about transmissible cancers in devils and do something to help save them.”