Parasitic Cancer: Paradox and Perspective

by Audrey Effenberger

Cancer. It’s a big subject, with a dizzying array of forms and manifestations that can affect all parts of the body. As populations around the world age, cancer’s prevalence will continue to grow, and it will become more and more important to understand and treat it. One lesser known variation is known as parasitic cancer. While its name may seem to combine two totally different ailments, understanding parasitic cancer can actually shed light on the concept of cancer altogether.


So what is cancer in the first place? On the most basic level, it’s abnormal or uncontrolled cell growth. The cell, the most fundamental unit of life, is a fantastically complicated and regulated machine of DNA, RNA, protein, and all kinds of molecules in between. When any part of the system fails, the entire system can be compromised. The mechanism by which this occurs is known as oncogenesis. Mutations in proto-oncogenes, or those that normally correspond with activating some part of the cell cycle, can transform the normal genes into oncogenes, resulting in abnormal proliferation of the cell. On the other hand, damage to tumor suppressor genes means that a repressing mechanism no longer works, and the cell will fail to stop or die at the appropriate times. Either of these mutations can lead to unwanted cell growth, known as a tumor. Most cells within a tumor are clones, having originated from a single rapidly dividing cell, so the tumor can be called a clonal population.

In fact, because mutation is a random process, the likelihood of a cell incurring a critical mutation in an important gene is quite low. Additionally, cells have various enzymes to proofread and repair DNA. The immune system works to recognize markers on the cell membrane and destroy misbehaving cells. Some tumors are relatively benign. However, no system of defense mechanisms is perfect. As people age or encounter carcinogens in the environment, the rate of damage can increase. Damaged cells that go unchecked can give rise to malignant and invasive tumors that spread throughout the body by traveling through the bloodstream, a process known as metastasis.


Though cancer can spread throughout one’s body in this manner, it’s thought of as a largely non-contagious disease. The only way in which cancer is “transmitted,” typically, is by transmission of a pathogen that increases the likelihood of developing cancer. In this way, cancer can only be spread indirectly.

Some bacteria damage tissues and increase risk of carcinogenesis, or cancer formation. For example, the H. pylori bacterium is known to cause stomach ulcers and inflammation that increase relative risk of gastric cancer by 65%.1 Viruses are another culprit; they damage the cell’s DNA by inserting their own and disrupting key sequences or triggering inflammatory responses that lead to rapid cell division. Known oncoviruses include Epstein-Barr virus, hepatitis B and C, and the human herpesviruses.2,3

Parasites, confusingly enough, can also cause cancer, albeit not the parasitic kind; for example, the Asian liver fluke is known to cause a fatal bile duct cancer.4 Again, however, all of these transmissible causes of cancer only increase risk; they can at most heighten the probability that the organism’s cells themselves will become cancerous.


Parasitic cancer is defined by its cause: the transfer of cancer cells between organisms. This is comparable to metastasis, when cancer cells migrate throughout the body. However, the new tumor originates from a tumor cell of another organism and is markedly, genetically different. As defined earlier, cancers are often clonal populations rising from a single abnormal cell. In the case of parasitic cancer, the new tumor is populated by clones of another organism’s cancer; therefore, parasitic cancer is also known as clonally transmissible cancer.

While parasitic cancers are very rare, examples can be found in a few animal species. These include devil facial tumor disease (DFTD),5 canine transmissible venereal tumor (CTVT),6 Syrian hamster connective tissue sarcoma induced in the lab,7 and a form of soft-shell clam leukaemia.8 Some cases of parasitic cancer have been documented in humans as well. While extremely rare, cancer cells can be transferred during organ transplants or pregnancies.9


Given the unique attributes of parasitic cancer, researchers can reframe their conceptual understanding of cancer and cell organization as a whole. All cells of a particular species have the same basic genetic information, but each cell may be slightly unique, just as human individuals have different eye colors or heights. We can extend the metaphor to bridge the macro- and microscopic. Every organism can be considered its own population of cells cooperating to sustain life, and most cells divide at a regular pace, correcting errors in DNA replication and preserving the overall homogeneity of the organism’s genome.

However, when a cell mutates and becomes cancerous, it changes notably. Given the known mechanisms of oncogenesis, similar types of mutations occur in specific genes to give rise to specific cancers; cells that are able to reproduce after suffering genetic damage have a different, stable genome of their own. Molecular analysis confirms this.10 All cancer of a certain tissue can thus be defined as its own species.11 This species reproduces, competes, and evolves. Tumors thus act as parasites on the rest of the population, sapping resources and occasionally causing direct harm. Benign tumors are analogous to “successful” parasites, coexisting indefinitely with their hosts, while malignant tumors eventually lead to the death of the organism.

The conceptual similarities and differences between parasitic cancer and parasitic organisms lead to important lines of questioning. This is seen in the vastly distinct effects of parasitic cancers on the aforementioned animal species known to have them. DFTD has devastated the Tasmanian devil population and could lead to extinction within three decades of the disease’s emergence, while CTVT has successfully coexisted with dogs for possibly thousands of years. Researchers speculate that reasons for this extreme divergence in outcomes are related to differences in the afflicted species’ genomes.5 Because the Tasmanian devil population lacks the genetic diversity that canines possess, their immune systems are less likely to recognize foreign cancer cells.

Furthermore, this immunological insight can be applied to human cases of parasitic cancer. For example, the genetic similarity between mother and child or transplant donor and recipient is naturally high or engineered to be; while this is necessary to prevent immune system rejection, it allows parasitic cancers more leeway to invade the body. Awareness of this can improve medical treatment in the future.

With the rapid advances in science and technology of the past century, physicians have gained a panoply of weapons to combat cancer. Modern cancer treatment includes everything from surgery to radiation and chemotherapy. However, these measures are imperfect. A paradigm shift spurred by the study of parasitic cancer may guide the medical research community’s efforts to cure cancer conclusively. By treating all cancers as distinct organisms parasitizing the body, physicians can approach treatment differently, combining immunological and genetic therapy with techniques similar to those used against invaders of other species. In this way, parasitic cancer is paradoxical in not only name but also action, and thus brings hope for the future of cancer research.

Audrey Effenberger ‘19 is a freshman in Greenough Hall.

Works Cited

  1. Peter, S.; Beglinger, C. Digestion. 2007, 75, 25-35.
  2. Moore, P.S.; Chang, Y. Nat. Rev. Cancer. 2010, 10, 878-889.
  3. Liao, J.B. Yale J Biol Med. 2006, 79(3-4), 115-122.
  4. Young, N.D. et al. Nat. Comms. 2014, 5.
  5. Dybas, C. Tasmanian devils: Will rare infectious cancer lead to their extinction? National Science Foundation [Online], Nov. 13, 2013. (accessed Oct. 4, 2015).
  6. Ganguly, B. et al. Vet. and Comp. Oncol. 2013, 11.
  7. Murchison, E.P. Oncogene. 2009, 27, 19-30.
  8. Yong, E. Selfish Shellfish Cells Cause Contagious Clam Cancer. Natl. Geog [Online], Apr. 9 2015. (accessed Oct. 4, 2015).
  9. Welsh, J.S. Oncologist. 2011, 16(1), 1-4.
  10. Murgia, C. et al. Cell. 2004, 126(3), 477-487.
  11. Duesberg, P. et al. Cell Cycle. 2011, 10(13), 2100-2114.



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