We had a seminar from Marco Restani of St Cloud State University yesterday — he’s a wildlife biologist who talked about Tasmanian Devils. Just a little tip: don’t ever invite wildlife biologists or conservation ecologists to give talks. They are the most depressing people in the world, and they really make it hard to hide away from the ugly realities. This talk was no exception: the Tasmanian Devil is in big trouble, and is facing at least two major threats, each of which may be sufficient to wipe them out. And just looke at that guy! He’s adorable! How can you let them go extinct?
The first big problem: the Tasmanian Devil is a marsupial with a limited range, confined to that large island south of Australia. They used to range over the entire continent, but were extirpated from the Australian mainland by, it is thought, the introduction of the dingo. Unfortunately, their refuge on Tasmania has been invaded by foxes (intentionally introduced by people Restani called “jerks”—I think, though, he was choking back some stronger language). This is catastrophic. There has been a major effort to kill off the foxes, but it may be too late, and they may have already established themselves.
The second big problem, and the one that I found particularly fascinating in a grisly, horrific way, is that the devils are being wiped out by serious new disease, Devil Facial Tumour Disease, or DFTD. It sounds awful and it looks worse.
This disease consists of rapidly proliferating facial tumors spreading across the jaws and face. It kills within months, and it’s spreading across the island at a frightening rate. Restani described some of his random sampling results; overall, about 16% of the devils have these lesions, with some areas showing infection as high as 40%, and others (particularly in the northwest) still disease-free. Think of this — tens of thousands of animals in Tasmania are covered with these lethal disfiguring lesions right now, and will be dying a painful death…before the foxes move in and take over their habitat.
Now I’ve got to really creep you out. This particular disease seems to be unique, with a very unusual cause.
The tumors have been examined cytologically. They, like typical cancer cells, have broken, rearranged chromosomes, exhibiting some fairly complex restructuring of the genetic material. They also have missing chromosomes. This is not at all surprising, and is what is seen all the time in all kinds of cancers.
The weird thing, though, is that all of the devil tumors have the same cytological scrambling. There are some slight differences, but they’re all traceable to small changes in the same common chromosomal reorganization. In addition, one animal was found with a marker in its normal cells that was not present in the cancer cells.
The explanation: these are all allografts. All of the tumors in all of the animals are descended from one original cancerous devil. Devils often fight over carcasses (they’re scavengers), and the idea is that the wounds they suffer are avenues for cancer cells to migrate from one individual to another and colonize and proliferate and bloom into full-blown DFTD.
Got that? It’s an infectious cancer. Cancer cells crawl out of one victim to infest another. It’s the same godawful cancer growing across the entire population.
While that is a chilling idea, it’s also fascinating. It’s a case where a cancer cell has acquired a little more autonomy and has graduated from an accidental, lethal killer of an individual to a kind of parasite that can leave its source host and thrive in others. I’m wondering whether it ought to be given a new species name of its own. Maybe we should be casting a more suspicious eye on HeLa cells, too.
What’s to be done to save the Tasmanian devil? One plan is to move animals to other island refuges. The problem right now is that there are no diagnostic tools to identify infected devils, and all you have to do is move one animal with incipient DFTD, and your refuge is infected. So the approach is to develop assays and, ideally, vaccines against the cancer.
This takes money.
You can donate as an individual — there is a fund set up and even us remote Americans can contribute. We can also make a case to our governments that this infectious disease is worthy of study, and that maybe we should be making an effort to understand this horrible creeping cancer now.
There’s another avenue for public pressure to work, too. Where did you first hear about the Tasmanian devil? Who has profited most from the devil?
Right. Warner Bros. and LooneyTunes. You’ve gotta love Taz. Now imagine Taz with painful, suppurating growths all over his face. Imagine watching the cartoons with your kids and having to explain that the Tasmanian devil is extinct, but Warner Bros. still makes a few bucks off the line of stuffed toys and the cartoons. It kind of takes the joy and the funny out of the shows if you think of the last Taz starving to death in the brush as an aggressive tumor consumes his face. Apparently, there is some Taz plush toy somewhere that Warner Bros. markets and gives a cut of the profits to devil research, but I haven’t been able to find it, and it’s not quite enough anyway.
It might be a good idea for a lot of people to hint to Warner Bros. that if they want a positive corporate image, here’s an opportunity for them to make a difference.
DFTD is horrible, but it’s not quite unique. Canine transmissible venereal tumour works the same way. I wonder how they’re able to avoid recognition by the host immune system.
Excuse me if this is a dumb idea, but can’t anything be done to cure these poor critters? Do the tumors respond to cisplatinum or any other chemotherapeutic agents? ?Would an animal that was cured of the disease then be resistant? Yes, I know, that takes more money to find out (donating, donating). Just wondering if anyone is researching that end of things.
Wow.
Thanks for this post, PZ. It’s chockablock with all kinds of crazy stuff I didn’t know before.
After reading about HeLa cells, I’m going to be much more careful with my discarded, er, biological matter.
Devils apparently went through a population bottleneck and have reduced MHC diversity, making them more accommodating to other devil tissues. CTVT is another case he mentioned, briefly, but I don’t know how CTVT gets around the canine immune system.
There is no treatment. Restani mentioned that in prior trapping surveys, they’d release the animals after capture…but now, when they catch a devil with DFTD, it’s euthanized. They’re vectors for the disease, you know.
One wonders whether these animals are so inbred that their immune systems simply don’t recognize these cancer cells as foreign or wether there is some mechanims involved that promotes the absence of an immune response. That would be very interesting, indeed.
But it seems to me that it should be relatively easy to establish a quarantine-based system of sanctuaries with healthy animals since this phenotype seems so easily recognizable. Now, catching the little buggers might be another problem altogether.
The DFT cells survive when allografted because of depleted MHC diversity in the affected Tasmanian devil population. There’s a nice paper on this transmissible tumor in the Oct 9 2007 PNAS (104:16221-16226) by Siddle et al.
“Excuse me if this is a dumb idea, but can’t anything be done to cure these poor critters? ”
Youre talking about eliminating a disease spread by virus in wild animals. That’s ridiculously hard. Think of how hard it is to eliminate virus-diseases in the human population – and we understand things like going to doctors and quarantining. In wild animals….if you miss even one, all your efforts were for naught.
Reintroducing varietal heredity into the population would be an essential long term program. The amount of zoos and private wildlife collections worldwide that contain Devils might be useful for impregnation of wild devils. It would be interesting to see if a genetically diverse population (one that has generations of separation from the current wild population) has the capability to take on the cancerous cells as an infection before even attempting to diversify the current wild genetic pool.
After doing some cursory digging, the only contact info for WB that seemed like it might be relevant is their customer service form:
http://www2.warnerbros.com/web/main/help/customer_service.jsp
There’s precedent for this. Jaguar the car company has established a trust for preserving jaguars the cats.
It’s not a virus.
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So the presence of foxes in Tasmania is now confirmed? I am getting angry. Really angry.
It’s not a virus.
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So the presence of foxes in Tasmania is now confirmed? I am getting angry. Really angry.
Forgive me, but: This isn’t a virus! PZ just got done telling us what it is. This is a cancer that is being spread from one devil to the next by facial bites. Cancer is a cell mass that originated as clones of one cell. A virus co-ops cells and cellular machinery to replicate itself. These things are pretty different from one another. Again, forgive me, but the distinction is important.
well Viggen, of course the two (virus and cancer) are not mutually exclusive. There are several viruses known to cause cancer (HPV, EBV etc)so you can not exlcude the possibility that the underlying cause is viral despite the fact that the transmission does not appear to involve a virus per se.
Those are wonderful questions, Dianne, and they really shine a spotlight on the interface between research and clinical practice. Every difficulty that you can imagine in getting a human population to comply with a health practice is compounded when you can’t even communicate with a group of patients, they’re not about to give informed consent, and “bite” or “flee and pee” are pretty much the total repertoire of their conflict-resolution skills. I read (Discover magazine, maybe?) about how wildlife biologists trying to give birth control to koalas had to be very careful, because those sweet-, cuddly-, torpid-looking animals bite like bastards when they’re caught.
Woodland Park Zoo in Seattle and San Diego (among many others) [ursine and other species reproductive measurement interventions], Washington State University [ursine cardiac and other physiological measurement interventions], and other institutions around the world are doing some pretty amazing things with conditioning to get animals to accept some interventions that were previously thought too intrusive for animals to accept. But you have to control their environment to such a degree to get them to do that, that the interventions have very little external validity for the wild situation.
As others have pointed out, miss just a few cases, and you’re right back where you started. It’s very complex, and yet, if we could get answers to the questions you pose, that knowledge would be invaluable. But it’s also true that at one point, human epidemiologists were no further along with their population than we currently are with wildlife. And interventions were able to be modified to low-resource situations (no lab-made alcohol fixative for a Pap smear in the bush? Beefeater Gin works really well as a substitute).
So while the optimal interventions are out of the question, I will eagerly watch to see what researchers with a bit of ingenuity will come up with in their place to study these questions.
By “accept”, I mean without general anesthesia, of course.
This may be an ignorant question, but hell, I’ll be the first to admit I’m nowhere near as educated as many that frequent this board. This is the first I’ve ever heard of a cancer moving between hosts, and I see from the later remarks that it was caused by this bottleneck in the Tazmanian population. Is the potential there for any cancers found in humans to become transmissible in the future?
If evolution has taught us anything, it’s that if there’s a niche, something wiill fill it, no matter how grisly or yucky from a human standpoint. (I remember learning that many people have almost-microscopic parasites living around the roots of our eyelashes. Squatters! How dare they?)
Others have blogged about the non-fatal Canine Transmissible Venereal Cancer. It was mentioned by Azra Raza at Three Quarks Daily and Ed Yong at Not Exactly Rocket Science) and before us all, Carl Zimmer at The Loom. It was written up in Cell* as the oldest known living cancer. Cell Press online also mentions that Tamanian Devil tumour might be another transmissible cancer. [I know that this comment will be delayed because of all the links, but I want to give everyone credit.]
To save the Tasmanian Devil, increasing the genetic diversity sounds like a good idea, but expensive and time-consuming. It will take time to identify candidate animals and arrange matings or investigate artificial insemination for TDs.
In the meantime, it might help to identify any areas of the Tasmanian Devil range that are not yet effective; and sling up a few fences to isolate them as much as possible from infected or partly infected areas. Fences are expensive, too, but people who know what they’re saving (a tourist draw, for one thing) might be willing to spend the money. Roads are a gap in the fence unless the public agrees to some kind of double-fence “airlock” system or bridges that are only down when there is traffic. And then hikers and hunters will cut holes in the fences unless there are gated stiles. But I think we’d be talking perhaps three fence lines in the whole island. Maybe one if there’s a heavily infected area that could be isolated to slow things down and give the other plans a chance.
I’m just brainstorming here; it’s probably not practical. But perhaps we could put our collective mind to imagining solutions and then seeing if any of them can be made practical.
*Reference: Murgia et al.: “Clonal Origin and Evolution of a Transmissible Cancer.” Publishing in Cell 126, 477-487, August 11, 2006. DOI 10.1016/j.cell.2006.05.051)
As a stopgap, I wonder if it’s possible to move a few uninffected TDs to an island off the shores of Tasmania? That supposes we can quickly develop a test (antibodies to the cancer?) for the cancer clone to check for exposure before symptoms appear.
Yes–that’s one applied reason why looking at answers to Dianne’s questions would be so important, in addition to the basic science knowledge gained.
Not really. You don’t need low MHC diversity to explain the Tasmanian Devil tumor. Cancer cells evolve readily to evade everything thrown at them including immune system attacks and surveillance.
Some human tumor cell lines have been shown to establish in other humans. HeLa cells during experiments years ago no one likes to talk about. Someone also managed to give themselves a tumor by a needle stick accident. But unless people start running around with syringes full of live cells sticking each other, not likely to happen.
Cervical cancer is a transmissible tumor but that is by transmission of oncogenic HP viruses. Not quite the same thing.
Raven, I agree that the risk is lower in humans than in species like devils and canines, but I don’t think you can say there’s “not really” any potential in the future–I think you’d have to know much more about the mechanisms of these forms of transmissible tumors to rule it out beforehand like that.
I agree it’s not as likely in humans as in those other species, but that’s not what zero asked.
Since when do human head and neck cancer patients frequently maul other humans during fights over carcasses? Probably not impossible but what is noteworthy about the canine and marsupial transmissible tumors is how rare they are.
The only cases of human transmission known are injections of live tumor cell lines. This is out of a population of 6.7 billion people.
A physicist here.
Does the fact that Tasmanian Devils passed through a bottleneck point to the same vulnerability in other species that have passed through bottlenecks (e.g., cheetahs)?
In other words, are species that have passed through bottlenecks more likely to have this kind of transmitable cancer?
Are simililar things seen in plants.
I have some stories about the Harborview ER I could tell…
But seriously, not so much. However, canine transmissible venereal tumor pretty much explains itself in its name, and last time I looked, humans were having lots of sex.
Unless you’re asserting that humans can never develop an analgous human transmissible venereal tumor, I don’t see how zero’s question about “potentially..in future” emerging diseases can be categorically ruled out.
Thanks for the responses guys. So pretty much the chances are zero, excluding the actual injection cases. What I meant by potential was more along the lines of cancers we see today mutating into much more virus-esque types of disease. Maybe I’m wording that poorly. The way cancers work now, is there anything to prevent them from evolving (years, 100s of years, etc) down the road into something contagious? I know cancers are mutating cells in the body, and from what raven was saying, only direct contact of cancerous cells with the cells of a second host can spread the cancer… but does that rule out cancer evolving into something altogether more dangerous, a cancer that is contagious through other mediums i.e. blood, saliva?
Mike: there are reports that Florida panthers, cheetahs and Asian lions also have low MHC variation. So one might assume that something like this could perhaps happen in these species as well, although I am not aware of any evidence for that. Of course a contributing factor here is the devils’ behavior. I think cats have much more developed rules of etiquette and don’t as much relish inflicting bodily harm onto each other
(see here: http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=10319256&cmd=showdetailview&indexed=google
Zero: that is an interesting question. First up, of course, most cancers cannot evolve. A cancer forms in your body and you either get rid of it or you’re dead. In either case a cancer’s life is relatively short.
Of course we know that a few cancers are caused by viruses, such as Epstein Barr and several of the papilloma viruses.
Now then would it be possible for a new virus to evolve that causes cancer by transforming cells in a way that would make them transmissable to other human beings ? It would seem highly unlikely given the way our immune system works. But if it would, how interesting. On might harness such abilties for all sorts of applications such as organ transplants etc.
We’ll save as many of the poor devils as possible, and nuke the site from orbit. It’s the only way to be sure. Plus we get rid of those weird Tasmanians.
Due to the higher radiation present when we re-introduce the survivors, they will have no trouble in re-invigoration their genetic diversity.
Of course, they might have a problem with the giant cockcroaches! Aye carumba, mate!
Colin
Carl Zimmer posted on CTVT and DFTD a while back: http://scienceblogs.com/loom/2006/08/09/an_old_dog_lives_on_inside_new.php
and it’s possibly more fascinating than DFTD.
The hypothesis that DFTD is virus related is not absurd. Zimmer quotes a paper saying, “[CTVT] represents the evolution of a cancer cell into a successful parasite of worldwide distribution.” I say we give it a new species name. After all, we’re going to need to make up for those global warming makes extinct.
As another example of how nightmarish cancer is, I’ve xenographed mouse cancer cells that were originally from humans into zebrafish and watched them develop into tumors.
#26 wrote, “First up, of course, most cancers cannot evolve. A cancer forms in your body and you either get rid of it or you’re dead. In either case a cancer’s life is relatively short.”
Not sure I can fathom what definition of evolve you’re using to exclude what cancers do. I study cancer from a molecular perspective and even single tumors are subject to natural selection (consider the HeLa cell line that’s been around since 1950). Many biologists even consider cancer to be an evolutionary disease.
I recall watching a documentary with footage of the poor infected devils, the poor beasties looked in pretty bad shape.
# 30: I would include the requirement of “being an organism” into what can and cannot evolve. A cancer cell, whatever it may turn into, dies with me. It does not have a life outside of me. (Unless you choose to keep it in an artifical environment by putting it in a culture dish. But that hardly qualifies. It does not have an evolutionary history of its own other than what is that of my species as a whole. And yes I know cancer cells change, and yes chemo and radiation probably constitue mechanisms of selection that give rise to a population of cells even more resistent to treatment. And yes, a virus cannot exist outside its host either, but it at least can migrate between hosts and have a life not tied to mine.
Seconded. Cancer cells can evolve within an individual, just like any other biological entity that can acquire and inherit mutations and compete with other entities for survival. I wrote a post about this subject a while back.
There are several viruses known to cause cancer (HPV, EBV etc)
True…
so you can not exlcude the possibility that the underlying cause is viral
…false.
I’m no biologist and will probably mangle terminology here, but: if Jane catches HPV, passes it on to Sue, and both of them develop cervical cancer as a result, their cancerous cells will be different. Jane’s cancer cells will have DNA resembling Jane’s other cells (albeit modified by the virus), and Sue’s will have DNA resembling Sue’s other cells.
This is not the case with DFTD. The tumour cells from different devils are identical, and in one case researchers found a devil who had a chromosomal abnormality in her own cells that was not present in the tumour cells.
http://www.abc.net.au/science/news/stories/2006/1711482.htm
As for humans, cancer can be transmitted via organ transplantation, although this is not a common occurrence. See e.g. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871995
Tasmania is not “that large island south of Australia”.
Tasmania, being an Australian state, is no less Australia that any other part, and it’s certainly not south of itself.
That’s the sort of thing that drives Taswegians nuts, and leads to Tasmania getting left off maps of Australia.
It is, however, “that large island south of the Australian mainland”.
Cheers PZ for highlighting the plight of the Devils, unfortunately not enough people know what is happening to the Devils, even within Australia.
The issue of the Foxes is interesting as I’m not 100% convinced that they are here. There have been carcases found and “sightings” however it could’ve been people bringing dead foxes over here for some reason and people mistaking feral cats for foxes.
Interestingly the Local Government here has set up a “fox task force”. They are both trying to prove that there are foxes and they have been given the task of removing them too. Some what of a conflict of interest, considering the multi-million dollar budget they have.
It took a great deal of political wrangling to get WB on board to help save the Devil, considering how much they have made out of Taz (and how they have made people spell Tasmania with a Z!!) they should be helping out far more.
They haven’t actually donated money btw, they have just allowed the Tasmanian Government rights to selling some Taz dolls in the hope that they may raise 200,000 dollars Aussie.
The Devils have been used as a bit of a political football too, with the Green Groups saying it’s farming habits and the forestry industry causing the tumors even when people knew that the tumors came a single animal and where passed by bighting.
Tasmania wouldn’t be the same without the Devils, I haven’t personally seen one in the wild, but I have been fortunate enough to hear them when I was camping down the South West.
It left me in no doubt why they where called Devils!
The Immortal Henrietta Lachs
I’ve been told that every once in awhile in the pre-Dispo days someone would be diagnosed with Henrietta Lachs carcinoma because of failure to properly clean glassware used to culture her cancer cells.
I live in Tasmania :) Don’t have much to add apart from that.
I agree that it’s completely unclear that are foxes are here, and certainly they aren’t doing any damage yet (as far as we know).
Of course it should be mentioned that there are plans to build the largest pulp mill in the world in Tasmania, which will double the amount of logging going on in the state, and puts a lot more habitat pressure on much of the wildlife of Tasmania. There was a study from Melbourne University a while ago that found that if logging continued in the area where the mill will be built, there is a 97% chance that the Wedge Tailed Eagle will become extinct in that area.
(Of course the fact that this mill will be pumping 64,000,000 litres of effluent into the ocean every day, burning wood to generate electricity, and releasing sulphur into the atmosphere is also concerning)
What experiments?
I am curious
It most certainly is possible for humans to develop some contagious cancer! Bluntly, if it can happen to dogs, it can happen to humans. If we’re really SOL, it might involve the respiratory system!
Do I expect it to happen anytime soon? Not so much, but it is something to keep an eye out for! Of course, if someone starts playing fast-and-loose with somatic-cell engineering or the like, the odds could change in a hurry.
I’m forwarding it to my brother – he’s got contacts at Cartoon Network (owner of the WB cartoons) and his wife works for AOL-Time Warner.
Way back in the 1970’s a herpes virus, H.Saimiri, discovered in spider monkeys, was found to be one of the most potent cancer-causing viruses ever. When it infected monkeys other than its normal host, it caused fatal lymphomas and leukemias within two months. It was 100% lethal to other monkeys. And its mode of transmission: airborne.
I don’t think it’s at all ridiculous to speculate that the cancer affecting the Devils could be caused by a virus.
Injecting them into human volunteer prisoners to see if they could cause cancer. They can.
Needless to say, this sort of thing wouldn’t be done today. At least not openly.
I’ve always thought of cancer as a great (if nasty) example of evolution– a lineage of cells, generally more prone to mutations and genetic change than normal cells, living ‘free’ in the body and taking advantage of whatever resources each can commandeer… In that population there is pretty intense selection for nasty traits like metastasis, recruitment of blood vessels (large tumours generally have low oxygen availability), and rapid proliferation. No wonder it’s such a miserable disease.
It all ends badly, of course, but evolution never looks ahead.
Evolution of cancer cells is what ultimately kills most cancer patients. We can deal with most primary tumors. But metastatic disease is much more difficult and most metastatic tumor types are considered 100% fatal. Quite often you see good responses to chemo, radiation, biologicals. It doesn’t last. Eventually the cells develop resistance to whatever you were treating with, including radiation, and when you are out of options, that is it.
This is somatic cell evolution, but so what? AIDS viruses do exactly the same thing in each patient, including evading the drugs one by one until none work.
This is one reason why the fundie attack on evolution is so horribly misguided. Evolution is something people in agriculture or medicine deal with every day that has direct effects on humanity. Metastatic cancer will ultimately kill 100 million of the 300 million people alive today in the US.
…and of course when the cancer can actually survive independently of the individual it developed in, then evolution really gets a chance to go to work.
Let no one say that Pharyngula does not recruit sacrifices for The Devil!
The other problem facing the (Tasmanian) Devil is that its species-wide crisis coincides with a global tsunami of extinctions approaching asteroid-collision levels.
We don’t hear much about this “Sixth Extinction”, even from scientists (“alarming loss of biodiversity” being the current preferred euphemism); not even from widely aware and vocal biologists such as our host here. As catastrophes go, Global Warming, dozens of individual species & diseases, and even the ozone layer have better press agents.
Meanwhile, we as a planetary biome are experiencing a “population bottleneck” of our own, and we as a species seem increasingly unlikely to avoid the same.
I think this topic remains relatively neglected for reasons including a non-trivial de-funding of ecological science in response to its political impact in the ’70s, but then again I’m a known sorehead.
#23
Does the fact that Tasmanian Devils passed through a bottleneck point to the same vulnerability in other species that have passed through bottlenecks (e.g., cheetahs)?
The discussion in the Siddle et al (2007) paper that I mentioned earlier mentions cheetahs and Hawaiian monk seals as populations that might be at risk for transmissible tumor spread because of low MHC diversity. Like many non-transmissible tumors (and in contrast to the DFTD), the CTVT evades the immune system by down-regulating cell surface expression of classical MHC class I molecules.
The Tasmanian devils in the affected region of Tasmania apparently have lower MHC diversity than inbred Gir (Asiatic) lions. Here’s the link for the paper-it’s Open Access at PNAS:
http://www.pnas.org/cgi/content/full/104/41/16221#42-
I don’t think it’s at all ridiculous to speculate that the cancer affecting the Devils could be caused by a virus.
Perhaps you should read the paper. How would a virus cause clonal tumors that are genetically and cytologically different from the host animals?
Ethical concerns about imminent extinction aside (not to minimize this tragedy):
Nobody has commented on a stunning evolutionary event that is implicit in this story:
DFTD and CTVT have (recently!) made a quantum jump from being ordinary SOMATIC CELLS to being transmissible DISEASE CELLS!
In one? generation, they went from being dependent subcomponents of metazoan bodies to being INDEPENDENT propagules. They have formed a new phylum!
Natura non facit saltum? Evidently not true!
Let’s clear up something here. DFTD is not caused by a virus, it is the cancer cells themselves that pass from one specimen to another. In effect, what you have is a sort of parasite infestation. And one which takes advantage of the close genetic relationship between specimens.
CTVT gets around the canine immune system by lacking many of the markers usually found on canine cells. This makes it difficult for a dog’s immune system to identify the cells as other. Though it does happen eventually, and the tumors get whittled down to more manageable threads of parasite tissue.
As noted by their names, DFTD is spread through biting, while CTVT is spread through genital contact. It should be noted that noted that not all devil biting is associated with conflict, devils will bite during play and courtship.
Another thing to note here about DFTD is that the tumors are often found with pus in them. It is possible that the patients are mounting an immune reaction, but not strongly enough to do them any real good. Providing anti-biotics and draining the tumor-cysts may make a big difference in the course of the infestation, but that would mean active intervention on our part. At the same time, not intervening means we lose the tasmanian devil. Well I say it’s about time we got over ourselves and took steps to save the species. We have the resources, and tasmanian devils are behaviourly prime candidates for domestication. If they have to survive as pets, then at least they’ll survive.
I wonder if environmental stress such as the introduction of the European Red Fox has increased the rate at which DFTD is spreading by reducing food for the Devils, and increasing competition and confrontation (biting) within the Devil population. Is there a way to increase food supply, without further upsetting the ecosystem, thus reducing confrontation? I know very little about Tasmanian Devils, perhaps they just like to bite.
One article I looked at reported the Devils down by 80% since the late 1990s because of the cancer, which created an open niche for the spread of foxes occurring at the same time. ( http://ecosystem-preservation.suite101.com/article.cfm/in_tasmania_feral_foxes_take_over ) I can’t help suspecting, however, that the foxes are more causative in the decline, despite what the article appears to be stating. Stress has a huge impact on the immune system. Did this disease immediately show up after the inbreeding hit MHC diversity? If there was a delay, why show up now?
I found a good article on bottlenecking and MHC diversity of native foxes on San Nicolas Island. ( http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=373489 ) Unless, I am missing something, the article seems to state that extreme bottlenecking is necessary for reduced MHC diversity. But according to the first article there was a 50,000 to 70,000 population decline of Devils since late 1990s, which unless there was an amazing recovery somewhere, doesn’t seem like an extreme bottleneck to me. Again, my question is why now if there isn’t something else going on? Sorry, I wish I had more answers than questions. I guess not much help. I hope something can be done to save the little guys. Personally, I am very fond of devils, sooo misunderstood. Thanks PZ, excellent articles, first time posting on your site. I am learning a lot.
Thanks PZ. I posted a link about this on another thread on your blog asking you to let people know about the plight of the Devil and you have. Praise be PZ. He anwers prayers.
Various Australian wildlife services made “hints” to WB about funding for research for years… and by “made hints” I mean “spent years begging on bended knee.” In return, WB has given a scrap of profits from a scrap of sales from the area that is related specifically to their one character, Taz! See what years of begging can get you? (I don’t think you’d get much more out of WB unless you made a *really* concentrated effort.)
Re: the discussion about “evolution” of cancer: I believe the distinction here is one of definition. Generally evolution is applied to discussions of changes that affect (at the least) populations of individuals. Variations, even due to mutation, in an individual (or, in the case of cancer, an individual’s individual cells) are not something I would consider to be evolution. A healthy population of a species (in this case, the Tasmanian Devil population is under considerable other constraints, including habitat limitations) would not likely be affected to this extent by something like DFTD.
efrique ( #35 ):
As it turns out, Australia is also a continent, and Tasmania is an island to the south of that continent. Why do you assume that PZ is speaking in political terms?
Kanaio ( #51 ):
Not having researched it, I would say that the bottleneck was most likely quite a while ago, and the population was probably down to a few dozen at the most. The cheetah bottleneck mentioned earlier, for instance, is estimated to have taken the population down to 12 individuals. As a result (from what I’ve heard; this is to my knowledge speculation without any concrete experimental evidence), any currently living cheetah should be able to accept skin grafts from any other currently living cheetah.
Also regarding cheetahs, but completely OT: they are gorgeous but fierce-looking animals. I had the opportunity (at the San Diego Wild Animal Park) to sit about 6 feet from one while one handler talked about them and another handler made sure none of us tourists got eaten.
#50-
Another thing to note here about DFTD is that the tumors are often found with pus in them. It is possible that the patients are mounting an immune reaction, but not strongly enough to do them any real good. Providing anti-biotics and draining the tumor-cysts may make a big difference in the course of the infestation, but that would mean active intervention on our part.
I suspect that the pus is related to a secondary bacterial infection of ulcerated facial tumors, since devils eat carrion and are continually exposed to bite wounds from conspecifics, regardless of tumor burden. The lack of MHC diversity won’t have any effect on the devil’s ability to mount an immune response against foreign pathogens; the problem in DFTD is that the tumor cells are recognized as “self”, and thus ignored by T cells that normally mediate an immune response to tumor cells. Tumor immunology is of considerable importance and relevance in developing therapies for human tumors…one of the reasons that xenograft tumor progression models in immunodeficient mice are out of favor with many cancer biologists.
The Siddle et al. paper addresses mixed lymphocyte responses in Tasmanian devils and the related Eastern quolls, because there was some evidence (from koalas and opossums) that the marsupial immune response might be indolent, or different somehow from that of eutherians. Another paper, which addresses devil lymphocyte phagocytic capability and mitogen responses in detail, was published recently in Developmental and Comparative Immunology ([snark]Behe’s favorite journal[/snark]) by A. Kreiss et al. (2007).
Doesn’t follow. “Phylum”, like all ranks except “species”, has no definition; it’s 100 % subjective.
And “species” has at least 25 often conflicting definitions, so some say it’s just as subjective.
Isn’t a cancer a population of cells…?
Not in geological terms.
Doesn’t follow. “Phylum”, like all ranks except “species”, has no definition; it’s 100 % subjective.
And “species” has at least 25 often conflicting definitions, so some say it’s just as subjective.
Isn’t a cancer a population of cells…?
Not in geological terms.
You could make a case that the TDFT is a speciation event. This tumor is behaving like any other pathogen, viral, protozoal, etc.. We aren’t used to thinking of mammalian cells as pathogens but so what. In this case, once one makes this viewpoint shift with justification, speciation becomes defensible. Ditto the canine case.
repost from PT:
On the fox question: are there *any* success stories for eradication campaigns like this? I’ve heard cases where introduced goats were successfully removed from Pacific Coast islands, but IIRC those were small, treeless areas.
Sorry for the long post and I rarely delurk but this touches me. I worked many years as curator of herpetology(amphibians and reptiles) at a large zoo active in international conservation. This is indeed a sad story, deserving of vigorous attention, but its just one with in a planatary disaster of extinctions. PZ is right about wildlife biologists being depressing. Our work brought us face to face with this dismal state of affairs every day. I remember feeling like we were bailing out a boat with a hole in the bottom. No time to fix the hole – just bail! The message was often depressing when making presentations to the general public, which drove the marketing people nuts. The zoo must always be a happy place. I recommend “Song of the Dodo” by David Quamen. That will depress you. But its full of evolution and its a great read.
Even if, in the unlikely event, a cure is developed, treating the entire population would be practically impossibble. How would you monitor the population for success? And while Australians have good experience with stringing fences(rabbits and all)the Tasmanian terrain may make that impractical.
A tactic employed by zoos, has been to maintain small populations of endangered animals in captivity as a hedge against extinction with the ultimate goal of reintroduction to the wild. As I remember, there are very few devils in zoos any where. Taking an appropriate number of devils into captivity until a solution for the wild population is found may be most effective. Zoos, including Australian zoos, have produced a tremendous amount of information on managing small captive populations of animals, including reintroduction techniques. It has really become a science in the past couple of decades. The cooperative effort between a number of US zoos and the US Fish and Wildlife Service for the recovery of the blackfooted ferret may serve as an appropriate model. As I remember, the ferrets have been a challenge in captivity, particularly with regard to desease control. I’d guess many of the protocols worked out for this program will apply to a similar effort for the devils. The American Zoo and Aquarium Association web site will be a good place to look. I’ll bet Australian zoos will have a similar site with similar information.
Every time a species is lost the richness, the stunning beauty of this place is diminished. I’ll never make it to Tasmania but if we loose the Tasmanian devil, it will, all the way over here in the middle of North America, just feel a little less special. I wish you great success and that’s fair dinkum, mate.
I have a serious question: Why should we care?
Extinction is a natural part of… Nature. Do we really care if one species goes or stays?
Sometimes I wonder why we try interfere with nature and keep some of these species on life support.
One thing we should of course be doing is initiating a massive fox cull. Be a good way to teach new Army recruits hunting and tracking, and give them practice in shooting straight. But amateur “conservationists” in Australia recoil at the thought of any hunting whatsoever, and the anti-gun lobby also froths at the mouth.
While this would not solve the problem of Devil facial tumour disease, it would at least help ease selection pressure, and it’s something we know how to do now.
1. Because it’s our fault (not the cancer, but the foxes and perhaps the bottleneck).
2. Because it would be a pity. Do you have no idea of the sheer awesomeness of Tassie devils?
1. Because it’s our fault (not the cancer, but the foxes and perhaps the bottleneck).
2. Because it would be a pity. Do you have no idea of the sheer awesomeness of Tassie devils?
Apparently the presence of foxes in Tasmania still isn’t quite confirmed.
(On the mainland, though, foxes have caused enough mischief…)
Apparently the presence of foxes in Tasmania still isn’t quite confirmed.
(On the mainland, though, foxes have caused enough mischief…)
Raven:
“But so what.” ??!
This was not just ‘speciation’! As commonly understood, speciation occurs when populations of a species are separated, then diverge over numerous generations until they become reproductively isolated. The result is a pair of phenotypically (behaviorally, physiologically) similar twigs at the periphery of the branching tree. Any taxonomist would put the two species in the same genus.
In this case, a taxonomist who is not aware of the history of the tumor-causing agents would put the transmissible pathogen somewhere among the “protozoa”: on an entirely different LIMB of the tree.
CTVT and TDFT represent single-generation macroevolutionary saltations of stunning magnitude.
Stuff that in the creationists’ pipe.
Raven #45 “Evolution of cancer cells is what ultimately kills most cancer patients.”
Not quite. It’s a combination of tumor burden and location than kills — meningiomas, which are benign (non-metastasizing) brain tumors can kill because they occur in sensitive locations.
“We can deal with most primary tumors. But metastatic disease is much more difficult and most metastatic tumor types are considered 100% fatal.”
Not quite accurate. The difference between primaries and secondaries relates to time before detection – given long enough, malignant solid tumors invade locally into blood vessels and lymphatics, seeding other tissues and establishing metastatic foci. This is analagous to PZ’s description of allograft spread between TDs.
Unfortunately, many cancers are simply found too late. There is also a subset of highly undifferentiated tumors dubbed PUOs (primary of unknown origin) that are so aggressive that the primary is sometimes never found and whose tissue of origin might not be identifiable.
“Quite often you see good responses to chemo, radiation, biologicals.”
Different tumors vary in their agressiveness and in their responsiveness to different agents. Seminoma of the testis, for example, is very sensitive to radiation, which is great news if the tumor is detected early.
The limiting factor on chemotherapeutic agents and radiation relates to their toxicity – chemo suppresses WBC and radiation damages healthy tissue. Once a tumor has spread, radiation of the primary is of no avail and it’s not possible to radiate all tissues to which metastases have spread – this is particularly true because many tumors metastasize to radiosensitive liver, brain, and lungs. (Happily lytic metastases to bone can be zapped for local control.) This is why metastasis necessitates a switch from radiotherapy to chemotherapy. There are a number of solid and hematologic cancers that are curable by chemotherapy.
“It doesn’t last. Eventually the cells develop resistance to whatever you were treating with, including radiation, and when you are out of options, that is it.”
Sometimes a subpopulation of cells is sensitive to the agent while other cells within the tumor are *already* resistant – treatment merely selects for that population that is resistant, while elimination of their competitors for nutrients actually provides a survival benefit. I suppose that you could call this ‘evolution’ of a tumor, but I think that this terminology is a stretch. It’s not so much that tumors are evolving resistance by altering their genetic makeup as they go along, it is more that resistant cells are given a survival advantage when sensitive competitors are killed off.
CTVT and TDFT represent single-generation macroevolutionary saltations of stunning magnitude. Stuff that in the creationists’ pipe.
I suspect the creationist response would be: “That’s not evolution, that’s devolution.” IME, most creationists (and not just creationists) fall into a sort of ranking fallacy, where a human is a ‘higher’ life form than a monkey and a mammal is a much ‘higher’ life form than a single-celled infectious organism; even if you can convince them that a species might ‘fall’ from mammal to microbe, that’s not going to persuade them that it can go in the other direction. (And to state the obvious, it certainly takes a lot longer to go in the other direction.)
I’m quite happy to view it as speciation, but I wouldn’t expect it to change a creationist’s mind; that would only work if they had a proper understanding of evolutionary theory to begin with.
Salient, you are mostly wrong on all points, so much that I’m not even going to bother to correct them all.
Tumor cells do evolve resistance to whatever we use to kill them. The mechanisms are well known, genetic mutations conferring resistance to chemo, radiation, biologicals. For radiation, it is mostly mutations in DNA repair systems, for chemo things like up regulation of the MDR pump, amplifications of target genes (DHFR, PALA), high Km mutations, uptake mutations, and so on. There is no difference from using antibiotics to treat a bacterial infection. After a while, inevitably they stop working because the bacteria have developed resistance to them. When the resistance mutations arise is irrelevant, they are mutations that confer a selective advantage under the given conditions.
Sure primary tumors might end up fatal if one sits and watches them for a while. We don’t do that. That is what surgeons and radiation oncologists are for. Figure it out, stage 1 and sometimes stage 2 cancers are considered curable. By the time you are treating stage 3/4, in most common tumor types you are just buying time.
raven #68
You misread much of what I wrote.
As for “that is what surgeons and radiation oncologists are for” I am a physician and spent three years working in oncology — both medical oncology radiation oncology. I quit the residency program only because I hated all the dying. Unless things have changed very much for the better, many tumors simply do not produce any clinical signs until they have already advanced. Some malignancies start out with such aggressive behavior that there is no way to stop them with treatments that would be effective in less aggressive tumors of the same tissue type.
Because that is quite a while ago, my knowledge of the molecular biology is out of date.
Here’s something recent that I’d already encountered that explains the clinically observed variation in tumor behavior: “Based on computational analysis of mutations affecting CAN-genes (candidate cancer genes) in breast and colorectal carcinomas, it has been estimated that cancers average 17 mutations (mostly SNPs) occurring within at least 90 genes.” (from, The Consensus Coding Sequences of Human Breast and Colorectal Cancers. Science. 2006 Sep 7)
Let’s compare bacterial infections with tumor cells. The population of bacteria has not arisen de novo at the time of infection, but are descendents of other bacteria. Cancers arise de novo through accumulated mutations in proto-oncogenes and tumor suppressor genes in an already existing cell line. The TD cancers appear to be acting more like ‘infections’ in that they are allografts of a single malignant line that do not arise de novo in response to mutagenic agents (which include viruses). I agree that bacteria evolve resistance, and that the sneaky little devils can pass genes for resistance horizontally to their buddies.
Are you saying that it has been demonstrated that those mechanisms you listed develop through *further* mutation in cells in which control of cell growth has already been lost through mutations in proto-oncogenes and tumor suppressor genes? In other words, that a cancer that was first detected to have 16 mutations is subsequently demonstrated to have 18 mutations? Or are you saying that it is known that those mechanisms provide the resistance found in resistant lines? Have Henrietta Lacks’ cells mutated further, for example?
This is an important distinction. If it is the first, then I’d have to agree that malignant cell lines do evolve. If it is the second, then I’d say that malignant cell lines ‘could’ be evolving and it just hasn’t been demonstrated, but that therapies do select for resistant populations in either case. If it is the second, it leaves us with the interesting question of why a tumor should have subpopulations of sensitive and resistant cells. I always wondered about that — perhaps you have provided the answer. Do you have any urls?
fyi, raven
Ability to acquire drug resistance arises early during the tumorigenesis process. Cancer Res. 2007 Feb 1;67(3):1130-7. Yagüe E, Arance A, Kubitza L, O’Hare M, Jat P, Ogilvie CM, Hart IR, Higgins CF, Raguz S.
“Resistance to chemotherapy is one of the principal causes of cancer mortality and is generally considered a late event in tumor progression. Although cellular models of drug resistance have been useful in identifying the molecules responsible for conferring drug resistance, most of these cellular models are derived from cell lines isolated from patients at a late stage in cancer progression. To ask at which stage in the tumorigenic progression does the cell gain the ability to acquire drug resistance, we generated a series of pre-tumorigenic and tumorigenic cells from human embryonic skin fibroblasts by introducing, sequentially, the catalytic subunit of telomerase, SV40 large T and small T oncoproteins, and an oncogenic form of ras. We show that the ability to acquire multidrug resistance (MDR) can arise before the malignant transformation stage. The minimal set of changes necessary to obtain pre-tumorigenic drug-resistant cells is expression of telomerase and inactivation of p53 and pRb. Thus, the pathways inactivated during tumorigenesis also confer the ability to acquire drug resistance. Microarray and functional studies of drug-resistant pre-tumorigenic cells indicate that the drug efflux pump P-glycoprotein is responsible for the MDR phenotype in this pre-tumorigenic cell model.”
Foxes definately are in Tasmania. A close friend who has hunted foxes saw a vixen with cubs on a recent business trip there. Another friend, his son, and the group they hunt with were paid by the Tasmanian govt. to take their beagles down to Tassie and hunt foxes…they got 25 in an afternoon, and several thousands of $$ each. The foxes are there…
I hate that this is happening to these adorable but fiesty animals!