Contagious Cancer Discovered: Dogs, Devils Hardest Hit

This shouldn't happen to a dog. A form of canine cancer has been found to spread from dog to dog through physical contact:

[T]he dog cancer, known as Sticker's sarcoma, is spread by tumor cells getting passed from dog to dog through sex or from animals biting or licking each other.

Because Sticker's sarcoma is usually not fatal -- and because some of the tumor cells reside in the dogs' genital tracts, where it's a small leap from one animal to another during sex -- today's worldwide distribution of Sticker's tumors represents a single colony of cancer cells, the new research concludes.

Indeed, scientists suspect that the colony, distributed among countless dogs, may be the longest in the world.

"I rather thought we might disprove this, but it came out the other way around," said Robin Weiss, of University College London, who led the study appearing in today's issue of the journal Cell. "It is clearly a dog tumor cell behaving absolutely like a parasite." Weiss called the tumor transmission trick "a curiosity of nature."

More bad news for fans of Warner Bros. second-tier cartoon characters: A similar, more lethal phenomenon seems to be infecting the legendary Tasmanian Devil. From Weiss' full article in Cell:

As a sexually transmitted cell, [canine transmissible venereal tumor] would not have been able to colonize dogs worldwide if it killed them too quickly; the host must survive in a fit state long enough to transmit the tumor, which in the case of females probably entails an estrous cycle. Thus, it will be interesting to model the restraints preventing the emergence of more aggressive subclones within the host and whether epigenetic factors affect the progressive and regressive phases of tumor growth. CTVT cells with their stabilized genomes may reflect kinship selection and reduced virulence, thus aiding host survival and onward tumor transmission (Frank, 1996), whereas the evolutionary dynamics of a "selfish," dead-end tumor typically progresses toward greater autonomy and malignancy (Greaves, 2002; Michor et al., 2004).

In contrast to CTVT, the Tasmanian devil facial tumor is highly virulent, killing most of the affected animals by obstructing their ability to feed (Pearse and Swift, 2006). If the devil facial tumor does not eradicate its entire host population, it will be interesting to investigate whether the newly emerged tumor cell lineage eventually evolves toward a less aggressive phenotype.

In the hamster and Tasmanian devil examples, the tumors spread among animals that have little genetic diversity (Cooper et al., 1964; Jones et al., 2004; Owen and Pemberton, 2006). The fact that CTVT is nearly homozygous in each of the DLA class II loci and also has closely related class I alleles may similarly have facilitated the origin and spread of CTVT within a partially inbred population, but today its chief reservoir is among mixed-breed dogs, particularly strays. Thus, CTVT is not a temporary, localized outbreak within a high-kinship group of animals; rather, it represents the evolution of a cancer cell into a successful parasite of worldwide distribution.

So the dogs appear to be living with this thing, while the ill-tempered marsupials may be in danger of extinction. "They fight a lot and have been spreading these facial tumors through bites," Weiss said. "The cancer cells clog up the jaw, and the poor animals die of starvation."

There have been no known cases of contagious cancer among humans (though transplanted organs have been observed to introduce cancer cells into their new hosts), so the only lesson for your own life may be that fighting and genetic purity never lead to good things.