Following a new PNAS paper regarding the strange facial cancers in Tasmanian devils, I have a post on the topic up over at Correlations. (Be sure to check out the Correlations homepage too!)
Tara – any insight as to why they are getting it less in Western than Eastern Tasmania? Is there a pool of genetically variant Devils, or is it an accident of the epidemic’s spread?
No idea. In the paper they looked at devils from the “north, east, and southeast” of Tasmania, and found them all to be genetically very similar at the MHC locus. I didn’t see them mention anything about western devils, but that would have been an interesting comparison–see if it’s spared them because perhaps they’re more genetically distinct? But then, last time I checked into it the north was relatively disease-free as well, so that suggests it the disease just hasn’t gotten a toe-hold in the west, I’d guess.
It sounds like a similar situation to Stickers Sarcoma which affects dogs. That is also a clonal cancer that is transmitted from animal to animal although it isn’t as aggressive as the Tasmanian one and so has managed to spread much more successfully amongst the dog population. Its believed to have originated in an asiatic dog, perhaps a husky, who lived over 1000 years ago.
Yep, it’s very similar to that–just newer, and doesn’t appear to be transmitted via sex as the dog cells are. They mention in the PNAS article the possibility for an evolution to lower virulence like the sarcoma, but it’s no new we’ll just have to wait and see.
I think it’s basically a case of geographic isolation, seeing as the tumour is only spread directly devil-to-devil. Don’t hold your breath for it to stay that way, while the relevant people in Tassie sit on their hands and commission surveys.
The facial tumours are de-facto sexually transmitted, by the way. Most of the transfer occurs from biting, which happens either during territorial encounters between mature animals, or during sex (devils are fairly vigorous in everything they do). The tumours take some time to develop, so there’s a possibility that the population could be sustained by young adults that have time to breed before they’re incapicitated. Not really an encouraging prospect, that.
I might be a bit out of date on this, since that’s from a talk I saw last year. I don’t think there’s really anything new happening though. Other than the looming extinction of the next-largest marsupial carnivore after the Tasmanian Tiger. I know a few people who are ropeable about the whole affair.
I’ve left a comment on your essay at correlations Tara. I was going to add an admonition here, but it looks like I’ll have to make an amateur’s informed response to matters raised in this thread.
First, it’s more accurate to think of DFTD and CTVT as parasites and not cancers. While the form each infestation takes is cancer-like, there is the fact that each is descended from cancer cells that appeared in an animal now long dead. That is, each cell line is what cancer researchers call an immortal cell line. And one capable of infesting other specimens of the original animal’s species.
CTVT appears most often in canine genitalia and adjacent tissues because that’s where exposure to the parasite occurs most often. Thus sexual contact accounts for the great majority of transmissions. Duration of contact may also play a role.
The course of the infestation is now well known. Tumors start to grow in the dog until some sort of limit is reached. At which point the animal’s immune system goes to work. The tumors shrink or disappear, with the end result being threads of parasitical cells laced throughout the host’s body. The patient then lives a normal canine life.
DFTD appears most often around the mouth and face because tasmanian devils bite a lot. They bite in fighting, they bite in seduction and sex, they bite in play. Tasmanian devils are mouthy animals, and may gain more information about their world through nerves in the mouth than by any other means. In any case, this behavior gives the parasite moer opportunities to infest a new victim and so the tumors show up where they do.
Some tazzies do appear to mount an immune response, but not all that effective. Being able to trigger a response more like that found in dogs could make a big difference. Something that shrinks or eliminate the facial tumors would certainly help, since thos tumors interfere with breathing, drinking, and eating. It should also be noted that these tumors also contain pus. They are, it would seem, sources of infection. As a matter of fact, the size of these tumors may be tied to such infections, and if these infections could be eliminated it would mean a reduction in the size of the tumors.
One last thing. In the DFTD genome a suite of genes has been found homologous to a suite of genes found in the CTVT genome. When you consider how long ago placentals split off from marsupials, the presence of a suite of genes so similar as those found in two different immortal gene lines becomes suspicious. In some early studies researchers reported that the tazzie parasite genes were identical with the corresponding canine parasite genes. The thinking appears to have gone in a different direction, but should research bear out the supposition that the two gene suites are identical, it has a lot of implications for eukaryote to eukaryote gene transfer. It would also mean that DFTD is in a very real sense the child of CTVT.
I left a response to Alan’s semantic quibble at Correlations, but I’ll mention a couple things here.
CTVT is unlike DFTD in that it survives by “down-regulating MHC class I and class II expression and upregulating nonclassical class I expression to avoid the natural killer cell response (10).“. This means that it has a much wider infection base. Most likely (IMO) it killed off any too-close relatives of its original host. Given Alan’s description (refs?) it seems plausible that metastasizing cells trigger an immune response while the original tumor doesn’t.
It would also mean that DFTD is in a very real sense the child of CTVT.
Not necessarily, IMO probably not. Depending on the material involved, it could have been grafted in by a retrovirus or bacterium that caused both cancers. Do you have a reference for this, I haven’t been able to find the paper with a quick search and don’t want to spend a lot of time if somebody else already has it.
I don’t think they have to be considered “either/or” regarding names. They *are* a cancer–they’re replicating cancer cells within an organism. But yes, they’re a parasite too–a separate life form living off a host. IMO, they’re both, but “parasitic cancer” seems redundant.
My source on similar genes in CTVT and DFTD goes back a number of years, and I can’t seem to find it again. A comparative study of the respective sets, and with analogous genes in normal dog and tazzie cells would be instructive.
Still cancers? Depends on how you define cancer. They are, after all, not something that arises from the patient itself, and they do have reduced, but stable, genomes. In the case of CTVT cells greatly reduced. The late stage behavior of CTVT infestation is also quite unlike most other cancers. Say rather that they are cancer descended.
DFTD is an example of the fact that not only is life weirder than we imagine, it’s weirder than we’re willing to admit.
Speaking of weird life, did you know there’s an amoebaform parasite evolved from a jellyfish?
They’ve even found it infecting (infesting?) humans!
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