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Question continued: UPDATE: After feedback, I’ve made the title more neutral.  The sensationalist tilt was unintentional on my part.  Thanks for those who provided input.  If you can’t agree to the wording now, you may simply delete your answer.  I neutered the question trying to make everyone happy.  This is obviously not possible.

Contagious means that that it’s observed to be transmissible by contact, causal, some agent is discovered, and the correlation reaches some sort of arbitrary threshold.  Viruses can cause cancer.  Fact.  However, there would have to be an underlying noticed vulnerability, noticed susceptibility, or opportunity.  What if we’re just not seeing it yet?  Some viruses barely come up on an electron microscope.  AIDS went unnoticed in blood banks.  We might not even know what we’re looking for in a chronic viral infection.

There is a preponderance of evidence that specific viruses predispose an individual to specific cancers in a statistically significant way.  It may not be 1:1, but that doesn’t mean it’s not contagious or never will be.  Common culprits include EBV — and various other members of the HSV family of viruses.

Answer by Tirumalai Kamala:

Do transmissible (contagious) cancers exist? Yes, but none discovered yet in humans. Best known examples are Tasmanian Devil facial tumor disease (DFTD) in Tasmanian devils, and Canine Transmissible Venereal Tumor (CTVT or Sticker’s sarcoma) in dogs. In humans, apart from accidental transfer during organ transplantation or other surgical procedures, example is limited to the rare Gestational Trophoblastic Disease (GTD). Are viruses implicated in such cancers? Not yet but as greatly more sensitive detection technologies are used to identify and enumerate the virome (viral communities in a body), they might be in future.

From Belov, Katherine. “Contagious cancer: lessons from the devil and the dog.” BioEssays 34.4 (2012): 285-292.

Evidence of transmissibility in DFTD and CTVT

  • Tumor genomes from different hosts are more closely related to each other than to their hosts
  • Tumors are serially transplanted between individuals through bites (in DFTD) or sex (in CTVT), even leading to epidemics
  • Form of natural transplantation since transplanted cancer cells are different (allogeneic), having originated in a different body

Tasmanian Devil facial tumor disease (DFTD)
Tasmanian devil is the largest carnivore marsupial, currently threatened with extinction due to DFTD.

From Belov, Katherine. “Contagious cancer: lessons from the devil and the dog.” BioEssays 34.4 (2012): 285-292.

  • Monophyletic (single ancestor) clonally transmissible tumor (Murchison et al 2010)
  • Schwann cell (neuronal) origin (Murchison et al 2010)
  • Spread by direct transfer of living cancer cells from bite of cancerous devil
  • Cancer first arose in a female Tasmanian devil; Subsequently spread through much of Tasmania
  • Diverged genetically during its spread; Appears to be evolving rapidly (Belov 2012)
  • Metastases common, present in up to 65% of cases (Loh et al 2006)
  • Could a virus be responsible? Per Murchison et al 2012, ‘Although DFTD is not virally transmitted, it is possible that a virus may have contributed to DFTD pathogenesis. We searched for the presence of virus DNA in DFTD by aligning virus-derived DNA sequences contained in the RefSeq database with the assembled DFTD genomes as well as the normal devil genome assembly. We did not find evidence for exogenous viruses in the DFTD genome. However, it is possible that DFTD contains viral sequences that were not detectable using this method‘. They looked but did not find evidence for virus with the caveat that the method they used may have missed detecting novel viruses.

From Murchison, Elizabeth P., et al. “Genome sequencing and analysis of the Tasmanian devil and its transmissible cancer.” Cell148.4 (2012): 780-791. Page on cell.com

Canine Transmissible Venereal Tumor (CTVT or Sticker’s sarcoma)

  • Thought to originate from a connective tissue cell type called histiocyte (Murchison et al 2009)
  • Genetic analyses show CTVT arose clonally (Rebbeck et al 2011)
  • Appears to exploit a unique mechanism called ‘host mitochondrial capture’ to avoid accumulating destructive mutations and to exploit the mitochondria’s metabolism (Rebbeck et al 2011)
  • Arose thousands of years ago in wolves or in some ancient dog breed (Rebbeck et al   2009)
  • Represents the oldest continuously passaged cell in the world (‘oldest recognized malignant cell line’)
  • Transmitted during sex; Occurs mainly as a lesion around the genitalia
  • Tumors appear within a couple of months; Metastases are rare, present in ~6% of cases (Das and Das 2000)
  • Both sexes get it; Seen in any kind of dog breed; On every continent (Das and Das 2000)
  • Initial progressive phase is marked by growth of CTVT cells that lack expression of MHC class I and II molecules
  • No lymphocyte infiltration of tumor initially
  • 3 to 9 months later, tumor either stabilizes or regresses
  • Regression coincides with considerable expression of MHC class I and II molecules on CTVT cells
  • Lymphocytes now infiltrate tumor
  • Tumor-host immune system dynamic can last a few months to several years, enabling tumor passage

Human Gestational Trophoblastic Disease (GTD)

  • Tumor of placental trophoblast cells
  • Trophoblasts express a mixture of maternal and fetal (allogeneic to the mother) antigens (proteins)
  • Tumor arises during or after pregnancy
  • Trophoblasts have unique capacity for tissue penetration and vascular re-modeling
  • GTD tumor cells have similar propensity
  • Not transmissible in classical sense
  • Transmissible in the sense that fetus-derived cells are the source of the tumor and they grow inside the mother


  1. Loh, R., et al. “The immunohistochemical characterization of devil facial tumor disease (DFTD) in the Tasmanian Devil (Sarcophilus harrisii).” Veterinary Pathology Online 43.6 (2006): 896-903. The Immunohistochemical Characterization of Devil Facial Tumor Disease (DFTD) in the Tasmanian Devil (Sarcophilus harrisii)
  2. Murchison, E. P. “Clonally transmissible cancers in dogs and Tasmanian devils.” Oncogene 27 (2008): S19-S30. Page on nature.com
  3. Murchison, Elizabeth P., et al. “The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer.” Science 327.5961 (2010): 84-87. The Tasmanian Devil Transcriptome Reveals Schwann Cell Origins of a Clonally Transmissible Cancer
  4. Murchison, Elizabeth P., et al. “Genome sequencing and analysis of the Tasmanian devil and its transmissible cancer.” Cell 148.4 (2012): 780-791. Page on cell.com
  5. Belov, Katherine. “Contagious cancer: lessons from the devil and the dog.” BioEssays 34.4 (2012): 285-292.


  1. Novinski, M. A. “Zur Frage uber die impfung der krebsigen geschwulste.” Zentralbl. Med. Wissensch 14 (1876): 790-791.
  2. Das, Utpal, and Arup Kumar Das. “Review of canine transmissible venereal sarcoma.” Veterinary Research Communications 24.8 (2000): 545-556. Page on www.uesc.br
  3. Murgia, Claudio, et al. “Clonal origin and evolution of a transmissible cancer.” Cell 126.3 (2006): 477-487.Page on els-cdn.com
  4. Hsiao, Ya-Wen, et al. “Interactions of host IL-6 and IFN-γ and cancer-derived TGF-β1 on MHC molecule expression during tumor spontaneous regression.” Cancer Immunology, Immunotherapy 57.7 (2008): 1091-1104. Page on nctu.edu.tw
  5. Rebbeck, Clare A., et al. “Origins and evolution of a transmissible cancer.” Evolution 63.9 (2009): 2340-2349.
  6. Rebbeck, Clare A., Armand M. Leroi, and Austin Burt. “Mitochondrial capture by a transmissible cancer.” Science 331.6015 (2011): 303-303.

Human GTD

  1. Wang, X., et al. “Immunobiology of gestational trophoblastic diseases.” International Journal of Gynecological Cancer 16.4 (2006): 1500-1515.
  2. Hoffner, Lori, and Urvashi Surti. “The genetics of gestational trophoblastic disease: a rare complication of pregnancy.” Cancer genetics 205.3 (2012): 63-77.