There are very few people today who have not been affected by cancer. It is a horrible disease for which there is no cure, only attempts at treatments (most of which are as toxic and as painful as the disease itself). The only positive aspect of cancer is that it is noncommunicable—you cannot contract cancer the way you could contract an infectious disease. Even if the cancer cells from another person managed to enter your body, say via a blood transfusion from a patient with metastatic cancer, you still would not develop cancer. That is because our immune systems are adept at targeting and destroying any foreign intrusion, including pathogens and cells from another person’s body. Unfortunately, this has not held true for Tasmanian Devils. They are one of the few species that is susceptible to a transmissible type of cancer: DFTD, or Tasmanian Devil Facial Tumor Disease. This transmissible cancer has been able to wipe out 90% of the population because of both the aggressive nature of the Devils, and their lack of genetic variability. Their aggressive nature manifests in frequent biting during feeding and mating, leading to large-spread contamination. If the Devils had the same genetic variability as humans, this disease would not have had the same devastating effects. However, when the Devils first arrived to Tasmania they experienced early population bottlenecking, a term for when a population experiences a dramatic decrease in size that results in a lot of inbreeding and an eventual lack of genetic diversity. Because of this, most of the Devils on the island have very similar genomes, making them more susceptible to this viral onslaught of cancer. So why should we care about cancer in Tasmanian Devils? Not only is this an ecological concern for Australia, but implications of this transmissible cancer could have profound effects on the current understanding of cancer in humans. For example, cancer is typically thought to arise gradually, as an accumulation of mutations that eventually lead to tumorigenesis, the formation of a tumor. For DFTD, however, a newer model is much more likely: chromothripsis. That long, confusing word describes the process where a chromosome (or chromosomes) is shattered and rejoined to the other chromosomes, resulting in significant chromosomal rearrangement from a single event. This theory is supported by the data from DFTD, and opens the door for a new understanding of the origins of cancer. For example, if some types of human cancer are caused by chromothripsis, then research should be shifted from broad genetic and environmental causes to the specific catalyst that causes the shattering. If shattering can be prevented, then so can this type of cancer. Another aspect of DFTD that is a point of interest for future studies is its transmissibility. DFTD has been so devastating to the Tasmanian Devil population because of its ability to evade the host’s immune system. This was first attributed solely to the lack of genetic variability within the Devil population, but further research presented by Deakin and Belov shows that the cancer cells might be actively evading the host immune system. They determined this by studying the Major Histocompatibility Complex (MHC). This complex, which is found on the surface of cells, is what allows the immune system to differentiate between “host” and “foreign”. In their experiments, the duo first gathered 4 Devils who had nearly identical MHC’s and grafted healthy facial tissue from one Devil on to another. The results were tissue rejection by the receiving Devil, indicating that although the MHC’s were extremely similar, the new host’s immune system was able to recognize the skin graft as foreign. They then took lymphocytes (a key cell type in the immune response, responsible for targeting and destroying foreign cells) from the healthy Devils and introduced those cells to cells infected with DFTD. In this experiment, there was no response by the lymphocytes, indicating that the DFTD cells were not recognized as “foreign”, even though they were. Although the actual mechanism of how they are able to do this still remains unclear, these results strongly indicate that DFTD is evading the host’s immune system, which results in the high death rate of this transmissible cancer. Hopefully, the next phase of research of this disease will focus on discovering the mechanism by which DFTD cells evade detection by the host immune system. This immune system evasion is why cancer is so deadly to humans. Even though our bodies are adept at targeting external threats, our immune systems cannot target cancer cells on their own because they recognize them as “self”. Recently, immunotherapy has emerged as a powerful new treatment of cancer. The basic idea behind this is to train the body’s immune system to differentiate between the healthy “self” cells and cancerous cells so it can attack the cancer cells, just like it is trained to recognize and destroy a virus. By studying DFTD to find out what allows those cancerous cells to evade the immune system, scientists could improve current human immunotherapy treatment. These two papers do an excellent job of documenting the progress of the disease and of proposing candidate genes that are involved in DFTD tumorigenesis. Epstein’s work shows that there is hope for the species in their rapid evolutionary response. Further studies could be conducted to identify what physiological changes make survival of the Devils possible. These rapid adaptations indicate that the Devils’ immune systems have rapidly evolved to detect and destroy any transmissible cancer cells, effectively rendering their evasion techniques useless. The implications of this research would be dramatic to the fight against human cancer: increased knowledge about a cancer cell’s ability to evade the immune system and about the Devil’s newly evolved immune response would create a greater understanding of how to counteract cancer cell’s evasion of the immune system in immunotherapy. The development of these treatments will lead to a more natural and personalized treatment of cancer that would replace the standard chemotherapies. Of course, current research is far from this point, but this devastating disease affecting Tasmanian Devils could be the next step in finding a better human treatment. REFERENCES Deakin, Janine E. & Belov, Katherine (2012). A Comparative Genomics Approach to Understanding Transmissible Cancer in Tasmanian Devils. Annual Review of Genomics and Human Genetics, 13, 270-222. Epstein, Brendan et. al (2016). Rapid Evolutionary Response to a transmissible cancer in Tasmanian devils. Nature Communications, 7, 1-7.