Tasmanian Devils are a fierce marsupial that live only on the southern Australian island of Tasmania. In recent years their population has been severely reduced by a dreadful invasive facial tumor that affects mostly males; the animals starve or choke to death, or are so weakened that they are killed by more-aggressive males.
All tumors in an individual are thought to start from one cell, though its descendants undergo repeated random mutations, some of which increase its invasiveness and survival ability. So when you look at the chromosomes in the cells of an individual’s tumor you see a characteristic pattern of chromosome breaks, recombinations, and deletions; a genetic fingerprint that distinguishes every individual tumor, even those of the same diagnostic type (that is, patient A’s melanoma has a distinct chromosome pattern from that of melanoma patient B.)
Drs. Pierce and Swift wanted to study the chromosomes of the Taz tumors to see if they could learn something about the origin of the disease. They trapped 11 animals, biopsied normal and tumor tissue, and looked at the chromosome picture, called a “karyotype.” The normal cells had 14 chromosomes each, XX or XY and 6 pairs of autosomes, the non-sex chromosomes.
But 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 (mashups of pieces of the missing chromosomes?)
Statistically there is no chance at all that this characteristic, highly mutated pattern arose independently in 11 animals. So: In all 11 animals, this is one and the same tumor! In other words, it arose once in one (long dead) Taz, and he transmitted its actual cells to another Taz, and so on and on.
We usually think this is impossible: After all, if I try to transplant my (normal or cancer) cells to you your immune system would reject them, because the target for rejection is a group of cell surface molecules called MHC, and MHC is so variable that the chances of yours being the same as mine are less than one in a million.
But there can be someone whose tissues you accept without any problem: your identical twin, who has the same MHC. Is it possible that all the Taz’s are identical twins? Of course not, they are born to different parents. But is it possible that the Taz’s are so inbred that they are essentially all identical? After all, they are a small unique population on an island with no input of new genes from immigrants. Although Taz have not yet been typed at MHC, a colleague of Drs. Pearce and Swift told them that when he mixed T cells and other white blood cells from random members of the Taz population together in cell culture, there was no activation of T cells in any case. Whereas if I did the same between cells of the members of our classes, in every case (unless we had a pair of identical twins!) there would be vigorous activation of T cells as they recognized the foreignness (to them) of the other person’s MHC.
The conclusion then is that the Taz population has become highly inbred and are thus passing a tumor from individual to individual which, instead of being rejected as a foreign graft ("allograft"), grows without restraint until it kills the recipient.
You can image, too, that if an infection arose that could kill one Taz it would kill them all. This, we think, is why we’re so diverse at MHC, which controls the extent to which we make immune responses; if one individual is susceptible, others will be resistant.
A.-M. Pearse and K. Swift. Allograft theory: Transmission of devil facial-tumour disease. Nature 439, 549 (2 February 2006)
