Decoding a Contagious Devil-Killing Cancer

Tasmanian devil with contagious cancer. Image courtesy Wikimedia

In the wilds of Tasmania and in labs in England, researchers are making some encouraging advances in their attempt to decode what may be a ticking bomb: an ugly, lethal cancer — a contagious one, a potential nightmare — that has been spreading among Tasmanian devils. As Ewen Callaway reports  today at Nature:

The first cases of devil facial tumour disease (DFTD) were detected in the mid-1990s, when people noticed the disfigured faces of devils in northeast Tasmania. These tumour cells pass from devil to devil when the aggressive marsupials mate and fight for food.

Once seeded, the cancer cells divide swiftly to form large malignant growths, and most infected devils die from starvation or metastases to vital organs within months. DFTD has marched steadily across Tasmania, and now a pocket in the northwest part of the island is the only place home to whole populations of uninfected devils. In the hardest-hit areas, more than half of devils are infected and many die as they hit their reproductive prime.

Four years ago, in Harper’s, David Quammen examined this plague in one of the most riveting pieces of science writing I’ve ever read. As he explains there, the Tasmanian devil outbreak raises the frightening possibility that other cancers could develop the capacity to spread much as colds or skin infections do. The key to how they do so would presumably be found in the DNA of the ugly tumors the devils develop on their faces. The cancer seems to spread when the devils, which bite each other on the face while fighting or mating, get a bit of tumor in their teeth. Somehow, it seemed, DNA or other material from those cancerous tumors caused the cancer to spread — a highly alarming possibility.

Now Callaway reports that a team led Elizabeth Murchison at the Wellcome Trust Sanger Institute in Cambridge, England, working on DNA from tumors in two different devils at opposite ends of Tasmania, seems to be narrowing the search for mutational culprits. They’ve identified about 1000 suspicious mutations in the tumor cells, including some identical to “mutations in genes linked to cancer in humans called RET and FACD2.”   By sequencing the genes in tumors in the two devils and comparing those with one another as well as with two healthy devils, they have filtered out a short list of about 1000 genes that seem unique to the tumors, and on these genes they and others will focus in research to come. they’ve also identified some genes missing from the devil tumors that are typically found in other cancers. As they do so, they’re getting a better read on how the devil tumors evolve. The short answer is fast; even though the cancer seems to have been around for only a couple decades, the tumors from the two devils at opposite ends of Tasmania differ significantly.

Murchison plans to sequence the genomes of more devils and tumours to get a better handle on the mutations responsible for the disease’s spread. With luck, the tumours will be caused by mutations that can be treated by the growing number of targeted drugs being developed to treat human cancers, she says. But it is more likely that genome sequencing could identify genes that are expressed by the tumour but not by healthy cells. A vaccine composed of the products of such genes could spur the devil’s immune system to go after the tumour.

Belov hopes to learn how the devil tumour slips under the immune system’s radar. One of the genes found missing from the tumour resembles genes that control T cells, which do not ordinarily enter the malignancies. “There is still so much that needs to be done to understand this dreadful disease. But the tumour genome will hopefully help us to get there faster,” she says.

In the meantime, the devils are fighting to stick around long enough to avoid decimation — and field workers are trapping devils in the wild to check their health and track the spread of the disease. As Quammen reported, this isn’t always an easy call. Here a biologist named Chrissy Pukk examines a devil, nicknamed Rudolph, to see how he fares:
Chrissy Pukk knew each devil at a glance.

Rudolph’s condition gave her pause. He was a two-year-old, nicely grown since she had first trapped him, his red nose healed . . . but there was something on the edge of his right eye. A pink growth, no bigger than a caper. “Oh shit,” she said. Tumor? Or maybe it was just a little wound, puffy and raw. She looked closely. She peered into his mouth. She palpated lymph nodes at the base of his jaw. The volunteers and I waited in silence. Evolution had shaped Rudolph for survival, and evolution might take him away. It was all evolution: the yin of struggle and death, the yang of adaptation, DFTD versus Sarcophilus harrisii. The leaping tumor, well adapted for fast replication and transmissibility, has its own formidable impulse to survive. And no one could know at this point, not even Chrissy, whether it had already leapt into Rudolph.

“Okay,” she said, sounding almost sure of her judgment, “I’m gonna give him the all clear.” She released him and he ran.

For the news, see Ewen Callaway (twitter), “Field Narrows in Hunt for Devil Tumour Genes,” Nature, 16 Feb 2012. Thanks to Callaway for corrections (above, struckthrough) to my original version.

For the deep background and one of the best and creepiest science stories you’ll ever read, see the peerless David Quammen,  “Contagious Cancer: The evolution of a killer,” Harper’s, April 2008. His book on the cancer, Spillover, should be out soon. You can also catch Quammen talking about the cancer on this very fine RadioLab segment, Devil Tumors.


  1. Why is man fighting so hard against evolution and extinction? The process has worked naturally for millions of years. Leave it to man to f things up.

      1. Aye, and it’s well probable that in an accident in paradise, it could very well be a matter of time before we’re in the same place.

      2. Absolutely positively maybe … also consider this:  Anytime there has ever been an infestation, mother nature has found a way to deal with it … and 6,991,514,234 people, sounds a lot like an infestation to me.

    1. I agree … mother nature has done a pretty good job so far … and consider this:  99.999% of all species that have ever lived on this planet, are now extinct.

    2. It could be that this cancer was introduced by a non-native species that was also introduced to the habitat of the Tasmanian Devil BY HUMANS and being that they have no natural protection or immunity to this cancer, this indeed would be our responsibility to prevent and try to solve.

    3. I see your point, roughly, but a great part of the concern, along with losing a species (that is already constrained by human activity; we’re already playing God), is in figuring out how a cancer can become contagious. That’s part of medicine, and when it comes to medicine, we decided a long time ago to ‘fight’ natural selection — or rather to improve our ability to survive it — by countering nature’s moves with our own. The hunt for the mechanisms behind this cancer is only partly an effort to save the Tasmanian devil. It’s an effort to save ourselves from a possible danger as well. 

  2. Its probably mutated due to mans use of chemicals or GM products or pharma ending up in the food chain of other lesser animals and is now causing horrible things to the planet. Nothing will be done about it and it will never stop because the free market and the corporate ability to do anything to make more money is more important than anything else. 

  3. So we should ignore that this contagious cancer may spread to humans? We should also ignore the fact that we could quite likely be a cause? And while extinction is a natural process since humans became the dominant species extinction rates have skyrocketed near mass extinction levels. Instead of preventing what humans do is screw up then try to fix it, if they can even be bothered…

  4. Who is to say that similar tumors could not be transmissible between people — if people routinely bit each other on the face? HIV is transmitted by certain behaviors and causes Kaposi sarcoma and predisposes to other tumors. Could the DFTD tumors contain a transmissible virus (as opposed to just mutated DNA)? With 1,000 or more mutations, at first glance it seems unlikely that newly developed targeted drugs are the answer to the problem, unless all the mutations are in the same gene for a growth factor or its receptor. And even then, with so much possible variation, could just one or a handful of drugs bind to the right site and inhibit whatever is wrong? DFTD is a fascinating problem.

  5. That’s funny, a few months ago there was an article about cancer and I wondered if maybe many of our cancers in humans are also contagious. I was practically laughed out of the forum and called an idiot.

    1. Well, you’re probably not an idiot, but to-date there has been no evidence of a cancer behaving like a virus or an infection, so it isn’t considered contagious.  It appears more and more that the genetic makeup of an individual makes them more or less vulnerable to the development of certain kinds of cancers.  Environmental factors also enter into it.

      1. Of course I have.  But HPV is a virus, not cancer itself.  It frequently can (but does not always) lead to the development of various kinds of cancer.  The “devils” in this article appear to be transmitting not a virus, but actual infectious cancer cells, which is significantly different than a virus which facilitates the development of cancer.

      2.  Aha, I stand corrected … I guess … but in the end, a highly contagious virus, that causes cancer … just seems like a slightly different mechanism, moving toward the same end.

      3. And you may be right, Fred.  I suspect that the researchers working with these poor “devils” may also be looking at the delivery mechanism for HPV, although they seem to have found a mutation with a direct mode of transmission that is very unsettling.

  6. It could be that this cancer was introduced by a non-native species that was also introduced to the habitat of the Tasmanian Devil BY HUMANS and being that they have no natural protection or immunity to this cancer, this indeed would be our responsibility to prevent and try to solve.

    1. The difference is that “contagion” allows a disease to spread from one being to another, regardless of family affiliations (sometimes, but more rarely, regardless of species).  What you’re describing is a predilection for developing cancer, usually caused by genetic factors.  My own family has that vulnerability, but not all members of my family have developed cancer.  In my family, those who smoke almost always get cancer, while those who don’t are less likely to develop that particular type of cancer.   

      1. In the case of the devils, the “predisposition” appears to be recent in origin, and so the question becomes how and why this came about.  I think those are amongst the answers they’re chasing. . .

  7. Nice post. Just a minor clarification. Murchison and her team could not determine the mutations that are unique to the tumour because they did not have non-tumour DNA from the first devil to succumb. The 1000 mutation figure is a back of the envelope calculation based on the ~136,000 single nucleotides unique to the tumour cells (these include germline mutations in the genome of the first devil to develop the tumour plus the new mutations in her tumour cells) less the ~135,000 single nucleotides that differ in the genomes of two devils. Murchison told me that it would take a “thousand tasmanian devil genomes” project to identify most of the natural genetic variation in devils and therefore untangle exactly which of the 136,000 mutations are new to the tumour (and potentially driving it). 

    Also, I should have been clearer in my story when I wrote about RET and FANCD2. The genes are linked to human cancers, but the mutations in the devil tumours have not been seen before.

    Can’t wait to read Quammen’s story! 

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