Tasmanian devils are now facing a second transmissible cancer, but both tumor types trace back to the same unstable chromosome.

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Rogue chromosome may be behind new contagious cancer striking Tasmanian devils

AUSTIN—The Tasmanian devil was nearly wiped out 20 years ago when a contagious tumor began disfiguring its face and killing animals by the hundreds. Since then, some individuals developed resistance and conservationists breathed a sigh of relief. But a second cancer has recently popped up in southeastern Tasmania—and it may reveal the Achilles’ heel that allows these cancers to develop, researchers reported here last week at the annual meeting of the Society for Molecular Biology & Evolution.

“Having two of these unusual tumors arise in such a short space of time really concerns me,” says study leader Janine Deakin, a geneticist at the University of Canberra.

The second cancer started showing up in 2014, when Tasmanian researchers discovered five Tasmanian devils with facial tumors. Like the first cancer, the tumors grew so large that they prevented the animals from eating. And, like the first, the cancer spread from animal to animal, as the devils bit and kicked each other during frequent confrontations. To find out whether the second cancer was related to the first, Deakin and colleagues performed a genetic analysis.

The original cancer was caused when sex chromosomes shattered. Some pieces attached themselves to one of the devil’s larger chromosomes—chromosome 1—and others rearranged themselves at various other spots in the genome, Deakin’s group reported in 2012. Chromosome 1 is also involved in the second cancer, she told meeting attendees, but the rearrangements elsewhere in the genome are not as extreme. In this second cancer, chromosome 6 is missing and instead has fused with chromosome 1.

The rearrangements may be due to an unusual configuration of telomeres, the caps at the ends of chromosomes that protect them from sticking to each other. Normally, telomeres get shorter with each cell division. But in Tasmanian devils, chromosomes passed on to offspring by the mother already have short telomeres; whereas those from the dad have extra-long ones. “It does seem that the shorter telomere may have something to do with the transmissible tumors,” says Deakin, as such premature shortening may make chromosomes prone to merging.

The odd telomeres may explain why the tumor gets started, but not how it infects other devils. The team’s analysis confirmed that, as with the first cancer, the tumor cells are not the infected devil’s own. Instead, they stem from a rogue cell that spreads from animal to animal as they fight.

One explanation for the rise of the new cancer is that chromosome 1 is particularly fragile. Unlike other chromosomes, it has rearranged its genes many times over the eons as marsupials, from koalas to opossums, have evolved. “It is hard to understand why such a weird feature would persist or would have evolved in the first place,” Deakin says.

Other researchers agree. “I’m fascinated by thinking about cancer as an evolutionary problem,” says Daniel Bolnick, an evolutionary biologist at the University of Texas here who was not involved with the work. In a sense, the body is a cooperative society of cells, and tumor cells are those that “cheat.” They look out only for themselves by hoarding the body’s resources to fuel unconstrained growth. In most cancers, the cheaters lose out in the end, because they kill the body they are cheating on. But these transmissible cancers not only evade the devil’s immune system, but are also able to move to new bodies and perpetuate. “It’s as if they are a new species,” he notes.

The tumors might also be the remnants of an old species, reported Laurent Frantz, an evolutionary biologist at the University of Oxford in the United Kingdom who studies the DNA of ancient and modern dogs. At the meeting, he showed just how well the canine version of a transmissible cancer has done for itself. Most modern dogs in the Americas descend from European stock and have very little DNA from the “precontact” dogs, which arrived thousands of years ago with the first people who walked into the Americas from Asia. But the DNA of the dog-transmissible cancer, CTVT, is very similar to that of the first American dogs, suggesting it arose early in American dog history. Today, this nonlethal tumor is found in dogs all over the world. “It’s the last remains of these precontact dogs that were all across the Americas for thousands of years,” Frantz said during his talk.

To date, the only other species with a transmissible cancer is a soft-shell clam. But, Bolnick asks, if such tumors have evolved in dogs, Tasmanian devils, and soft-shell clams, “Where else are we going to start to find them?” 

*Update, 19 July, 3:58 p.m.: This story has been updated to emphasize that these comments are from Frantz’s talk and not an interview.