Tasmanian Devils Are Becoming Resistant to Species-Ending Infectious Cancer

There are good reasons that transmissible cancer isn't really a thing. This mostly has to do with the immune systems of advanced organisms—while our own cancer evades immune responses by virtue of being, well, part of us, cancer from other individuals is recognized as an invader. Thus, outside cancer is quickly rooted out and eliminated. Cases of transmissible cancer in humans are extreme novelties, occurring rarely in immunocompromised patients, such as those with HIV.

In nature, a few species are unlucky enough to have infectious cancer as an everyday threat. Shellfish get it thanks to weak immune systems and an existence based on the constant ingestion and filtering of seawater shared by other shellfish. Dogs get it thanks to the swapping of tissues that occurs in rough dog sex. Tasmanian devils get it because of the tissue swapping involved in constantly fucking up each other's faces. That's a prerequisite for transmissible cancer occurring at all: the transmission of full-on tissue. A cancer cell doesn't behave like a bacterium or virus—cancer needs to be transplanted en masse for it to gain footing elsewhere.

In most cases, devil facial tumour disease (DFTD) is fatal. Over the past two decades, some 80 percent of the entire Tasmanian devil population has been decimated by the cancer. The disease has spread across nearly 95 percent of the island of Tasmania and has affected all known devil populations. Epidemiological models have predicted that DFTD likely portends the end of the entire Tasmanian devil species.

There may be hope, however. No, the devils don't seem to be learning to interact socially without destroying each other's faces, but their immune systems are learning to fight back against the infection via phenomenally rapid adaptations. This is according to a paper published on Tuesday in Nature Communications by disease ecologist Andrew Storfer and colleagues at Washington State University.

"Overall, our results reflect a rapid evolutionary response to this strong selection imposed by DFTD, and such a response to a highly lethal, novel pathogen has rarely, if ever been documented in wild populations," Storfer and co. write. "The only other well-studied example, the evolution of rabbit resistance to myxomatosis following its release in Australia, took place over a much larger number of host generations."

The swapping of tissues is a necessary but not sufficient condition for transmitting cancer. There is still the issue of immune responses. What helps DFTD is that Tasmanian devils all happen to look pretty similar genetically. This is the result of various "population bottlenecks" occurring through the species' history. At various points, the species shrank to a very small population size, which then recovered to normal levels. The effect is that the post-bottleneck devils all descend from a relatively small number of ancestors.

Because DFTD is fairly new, Storfer and his team were able to compare DNA from Tasmanian devils from before its emergence (based on archived tissue) with DNA from devils alive eight to 16 years after the disease appeared. Genetic variations began appearing in as few as four generations of the animals, which is remarkable given that rapid evolution usually requires some amount of pre-existing genetic variation, which the devils don't really have.

The researchers found five genes in two regions relating to cancer or immune function that are likely indicative of genetic selection. "The functions of these genes suggest that the devil immune system may be adapting to be able to recognize tumour cells," the paper notes. This functionality will need to be fleshed out further in future research.

This gives hope for the devils not just in their own adaptability, but because we may be able to incorporate the genes into captive populations that may one day be necessary for repopulation efforts. "First and foremost, this gives us hope for the survival of the Tasmanian devil," Storfer offered last week in a press briefing.

The findings may also have implications for wildlife disease in general and also human cancer. "Because this cancer moves from host to host it's effectively like one very long-lived human tumor within a single individual," he explained. "This may give us some insights into cancer recurrence and remission in humans."