Contagious Cancer, Beyond the Devils
Few health issues strike a deeper chord of fear than that of cancer—your own body’s tissues being hijacked, turning against you and taking over. An estimated 1,596,670 new cancer cases (not including some types of skin cancer, which are not reported to the same registries as other cancers) will be diagnosed in the United States this year, and about 571,950 people will die from cancer during the same time. Roughly 11.7 million Americans alive today either have cancer or are in remission from it (see here for source of those statistics and more information).
In other words, cancer is a huge concern, and rightly so. With only a few exceptions (human papilloma virus, HPV, which causes cervical cancer, being the most prominent), though, humans don’t worry much about catching cancer from one another. The fear of cancer is of one’s body (and lifestyle) betraying oneself, not of being infected by another person—such as with the fear of AIDS, MRSA, the flu, or any of a number of other infectious diseases. Just the thought of a rampant epidemic of disfiguring tumors seems like the stuff out of a horror movie.
Unfortunately, just such a thing has become a reality for a mammal that is struggling in the fight against extinction. Much press has (rightfully) been given to the grotesque epidemic of contagious cancerous tumors that is currently decimating the remaining of the Tasmanian devil ( Sarcophilus harrisii ), which, even prior to this outbreak, already faced critically shrunken numbers due to habitat destruction and the introduction of non-native mammals to their home on the island of Tasmania. It doesn’t help that the social dynamics of the devils—they bicker and bite each other fairly often—are only hastening the spread of this devastating cancer. McCallum et al. (2007) predicted that, if the trends seen in transmission and mortality of this cancer continue, the devils could be extinct in 25-35 years. As those authors point out, the ultimate prognosis for the species does depend on factors such as latency periods of the tumors and population densities in the remaining clusters of devils, and ongoing monitoring is of utmost importance.
While the issue itself is disturbing—a rare species being wiped out by a new and aggressive disease, exacerbated by its own irascible behaviors—it raises another issue of concern: how unusual is it for cancer to be transmissible, and are other rare species at risk of tumors that can be transferred between individuals?
There are indeed other examples of transmissible tumors. One prime example is canine transmissible venereal tumor (CTVT), a histiocytic tumor that is passed between dogs through sex as well as sniffing and licking of the genitals. At one point it was thought that a sexually transmitted virus, similar to HPV, caused this disease. It turns out, however, that it is the CTVT cells themselves that are infectious, not a virus that activates them. The cancerous cells themselves, which are essentially clonal, are what is passed from animal to animal.
For example, when an infected Dog A has genital contact with Dog B, what is transmitted is not some agent (such as a virus) that triggers Dog B’s cells to start dividing and creating tumors. Instead it is the cancer cells themselves, which are genetically different from both Dog A and Dog B, which continue to clone themselves on their new victim. Thus it seems animal that receives CTVT from its mate is not so much infected as colonized, and that is why CTVT is sometimes referred to as a “parasitic cancer.” The tumors most often appear on the external genitalia, but may also affect the nose and mouth.
There are few interesting aspects of CTVT cells. While normal dog and wolf cells contain 78 chromosomes, the tumor cells have fewer, usually between 57-64, and even those chromosomes bear some distinct morphological differences from those found in healthy dog tissue. The disease also infects coyotes (which also have 78 chromosomes) and red foxes (with only 34 chromosomes). The tumors can spontaneously regress (Chu et al. 2001), and domestic dogs are sometimes treated with chemotherapy (Scarpelli et al. 2008).
Where and how did these contagious tumors arise? A study by Rebbeck et al. (2009) showed that CTVT first appeared in either a wolf or domestic dog, most likely from east Asia, over 6,000 years ago, although it appears the common ancestor of all extant tumors may have arisen as recently as 200-2,500 years ago (Murgia et al. 2006). It has been hypothesized that low genetic diversity in a population is a strong factor in the appearance of transmissible tumors (McCallum 2008). Dogs are not lacking for genetic diversity at the moment, but it is thought that CTVT arose in a small, inbred population, and that emergence helped it to get a metaphorical foot in the door to subsequently spread amongst other canines (Murgia 2006). Fortunately for canids (unlike the hapless Tasmanian devils), CTVT is not a critical conservation issue and does not pose a threat to any species at the moment.
There are currently only three transmissible cancers known to medicine: the Tasmanian devil facial tumors, CTVT, and a sarcoma that arose in lab hamsters in the 1960s, which is transmitted via mosquito bites (Banfield et al. 1965), or, in the absence of mosquitoes, subcutaneous needle injections by humans (Fabrizio 1965).
As of yet there are no human cancers that are directly transmissible, with the very slight exception of a surgeon that accidently injected a patient’s histiocytoma into his hand during an excision surgery (Gartner et al. 1996). So, while the issue of an epidemic of a highly fatal, contagious parasitic cancer would indeed be a nightmare scenario, it seems that as of now humans are in the clear—though the Tasmanian devils may not be as lucky.
Banfield, W. G., P. A. Woke, C. M. MacKay, and H. L. Cooper. 1965. Mosquito transmission of a reticulum cell sarcoma of hamsters. Science 148: 1239-1240.
Chu, R. M., C. Y. Lin, C. C. Liu, S. Y. Yang, Y. W. Hsiao, S. W. Hung, H. N. Pao, and K. W. Liao. 2001. Proliferation characteristics of canine transmissible venereal tumor. Anticancer Research 21: 4017-4024.
Fabrizio, A. M. 1965. An induced transmissible sarcoma in hamsters: eleven-year observation through 288 passages. Cancer Research 25: 107.
Gartner, H.V., C. Seidl, C. Luckenbach, G. Schumm, E. Seifried, H. Ritter, and B. Bültmann. Genetic analysis of a sarcoma accidentally transplanted from a patient to a surgeon. _New England Journal of Medicine _ 335: 1494-1497.
McCallum, H. 2008. Tasmanian devil facial tumour disease: implications for conservation biology. Trends in Ecology and Evolution 23: 631-637.
McCallum, H., D. M. Tompkins, M. Jones, S. Lachish, S. Marvanek, B. Lazenby, G. Hocking, J. Wiersma, and C. E. Hawkins. 2007. Distribution and impacts of Tasmanian Devil Facial Tumour Disease. EcoHealth 4: 318-325.
Murgia, C. , J. K. Pritchard, S. Y. Kim, A. Fassati, and R. A. Weiss. 2006. Clonal origin and evolution of a transmissible cancer. Cell 126: 477-487.
Rebbeck, C., Thomas, R., Breen, M., Leroi, A., & Burt, A. (2009). ORIGINS AND EVOLUTION OF A TRANSMISSIBLE CANCER Evolution, 63 (9), 2340-2349 DOI: 10.1111/j.1558-5646.2009.00724.x
Scarpelli, K. C., M. L. Valladao, and K. Metze. 20010. Predictive factors for the regression of canine transmissible venereal tumor during vincristine therapy. _ Veterinary Science_ 183: 362.