The Tasmanian Devil (TD) is threatened by a dreadful outbreak of facial tumors, which grow rapidly and kill the animals as they become unable to defend themselves and feed. There are fears that the entire population of this unique fierce, wolf-like marsupial may be lost.Drs. Pearse and Swift captured 11 animals and biopsied the tumors, as well as normal tissue. They first described the normal TD karyotype: 14 chromosomes (6 pairs of autosomes and XX or XY).
To their surprise, all the tumors had exactly the same, and a very abnormal karyotype: 13 chromosomes total, but neither copy of chromosome 2, no X, no Y, and 4 additional chromosomes which could not be definitively identified. One animal had an inversion marker in all his normal cells; it was not found in his tumor.
In humans, certain malignancies have a characteristic chromosome break or transposition, but in addition, each patient’s tumors acquires its own particular chromosomal abnormalities. Nothing remotely resembling the condition with the TD has ever been described.
Their conclusion is that all TD have the same tumor, which they are passing from animal to animal. Since they are highly aggressive, encounters often result in biting, and the most likely place for one to bite another would be on the face. It is at that time, probably, that tumor cells are transplanted from one to the other.
Why are the tumors not rejected by the recipient’s immune system? They point out that the TD population shows little genetic heterogeneity, as might be expected when all animals live in a small continuous area like the island of Tasmania. They are all, in other words, closely related.
A colleague of theirs has told them that when one-way MLRs are performed between random members of the TD population, almost no proliferation of T cells is seen is response to MHC on the other animal’s macrophages; just as you’d expect in an essentially-inbred population. So the tumor is not recognized as foreign…
This is about the most dramatic evidence I've seen in favor of being as diverse as possible at MHC loci.
A.-M. Pearse and K. Swift. Allograft theory: Transmission of devil facial-tumour disease. Nature 439, 549 (2 February 2006)
4 comments:
So my question is this...if identical twins are separated at birth, what are the chances that if one develops a certain cancer, that the other one will develop the same cancer?
Another way of asking this is, will Tazmanian Devils that live in zoos around the world develop the same cancer? Or is there a large environmental aspect?
As I see it, the cancer must be "caught" from another Taz by direct contact. The genetics come in to allow it to be caught. So I wouldn't say that the animals are predetermined to get the cancer, but that their genetic homogeneity predisposes them to get it if it is in the environment.
As to identical twins, if the cancer has a large hereditary component, I'd guess the incidence in the second twin would be high. That's true in retinoblastoma, though there are discordant monozygotic twin pairs, too, in which the mutation must have occurred after the embryo split into two twins.
What jjc7630 makes mention of is the capacity of an individual's cells to acquire capabilities that would lead to abnormal cell proliferation and maintenance, transforming normal cells into malignant cancer cells. In this case, the normal cells of the TD are being transformed via an extrinsic mechanism (what jjc7630 means by ‘being caught’). Therefore, it appears that the cancer is introduced via the environment, and the body of the TD 'allows' for its expression. With identical twins then, who are genetically identical, I would think that they both have the same capacity for such change and would be affected in the same manner when introduced to the cancer-causing substance. We know that cancer alters the genome of a cell, yet concerning the TDs, could their evolution in close proximity have resulted in a widespread change in their genome, thus making them susceptible to the tumor-causing agent that was not recognized as foreign? …or is their susceptibility a 'normal' part of a TD's genome, meaning that any TD would suffer the same change when introduced to the genome-altering source?
Could there be a genetically engineered solution to this problem? Make a stronger TD, breed it and release the genetically altered offspring. Or, how hard would it be to round TD's up, kill the infected ones, and release the non-infected ones? This would be akin to the UK's response to Hoof and Mouth disease.
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