Populations of Tasmanian devils have quickly decreased by 80% over the past 20 years. A highly contagious cancer has taken hold over many populations, ending the lives of devils before they grow old enough to produce many, if any, offspring. Devil facial tumor disease is very unique in that its cancer cells are highly transmissible between individuals. Because Tasmanian devils are very aggressive, their social and mating interactions often involve fighting and bites to the face. When an infected devil encounters an unaffected devil in a fight, the mutated cells are able to spread to the open wounds of the unaffected devil, thus spreading the cancer.
The cancer originally arose from a mutation in a single Tasmanian devil in the 1990s. It grows on the devil’s face, particularly around the mouth. Large tumors can deform the skull or jawbone of a devil, as it places much pressure over the area it resides in. This makes it incredibly difficult and painful for the devils to eat. Tasmanian devils usually die from either the cancer itself or starvation in less than 6 months.
The reason as to why this particular cancer is so contagious is because of its lack of major histocompatibility complex (MHC) found on the cancer cell’s surface. The MHC found on foreign cells allows the immune cells in an individual to detect the cells as foreign objects. Because of the lack of MHC on the devil cancer cells, the immune cells of an affected devil are unable to read the cancer cells as foreign objects, and therefore the devil’s immune cells do not attack the cancerous ones.
However, the decline of Tasmanian devils has slowed somewhat over the past few years. One of the possibilities for this is that Tasmanian devils have started to evolve a genetic resistance to the cancer. To find out more about this possibility, an evolutionary geneticist named Andrew Storfer sequenced 1/6th of the devils genome using 294 individuals from 3 different populations. He discovered that among an increase of five variations of genes among recent devil populations, two of them, CD146 and THY1, assist the immune system in recognizing foreign objects. It is likely that a resistance has evolved in one or both of these genes, resulting in a greater immune response to devil facial tumor disease and therefore slowing both the spread of the cancer and decline of Tasmanian devils. Though Storfer cannot test this hypothesis on physical Tasmanian devils due to their endangered status, he will continue to research the interactions between these two genes and the cancerous cells in the lab to determine if there is stronger evidence to support this hypothesis. This research is extremely important to the continued existence of the Tasmanian devil species. If this hypothesis is true, then Tasmanian devils can make a comeback without human involvement, while scienctists can focus conservation efforts elsewhere.
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