The sexually transmitted dog cancer that could tell us how tumours develop

The mutations of canine transmissible venereal tumour (CTVT) promises to show how the tumours develop and respond to environmental pressures.

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Not even Lassie could have seen this coming. As you contemplate the bleakest bits of the cancer report issued by the World Health Organisation on 3 February, take heart: recent research suggests that the genitals of the world’s dogs might offer clues for fighting the war on cancer.

Cancer is mainly a disease of longevity, and as the global population grows and ages, the incidence of cancer is on the rise. As the World Cancer Report puts it, “The worldwide burden of cancer remains huge and is escalating.” There is no quick fix: advanced cancers, or those that have metastasised, are “mostly intransigent to treatment”, and encouraging a healthy diet is likely to have only “modest” effects. “Billions of dollars,” the report argues, “are riding on the premise that personalised medicine and targeted therapy will come to the rescue.”

As luck would have it, newly published research offers an 11,000-year-old Spitz as a rescue dog. It was a fair size, with a mostly black coat and a face not dissimilar to today’s Spitz dogs. Its genes were a mixture of wolf and more modern canines. We know all this because a tumour grew in the dog’s body. It’s the same tumour that is infecting dogs all over the world today, and its genome offers clues to how tumours take over the body – and why sometimes they don’t.

Genetic scientists report that the canine transmissible venereal tumour (CTVT), found in dogs all around the world, is the same organism that first came into existence in that unlucky dog 11,000 years ago. Researchers at the Wellcome Trust Sanger Institute in Cambridgeshire documented its genome and published the results in the journal Science.

CTVT is one of only two naturally occurring transmissible tumours; the other one grows on the face of the Tasmanian devil. CTVT is transmitted through mating and other activities that allow cells to slough off one dog and embed in the tissues of another. This is probably not the bit to dwell on (look on the internet for images of CTVT and you’ll agree). What is interesting is that the tumour has modified significantly over the millennia.

Examining these mutations – and comparing them with the mutations that are slowly wiping out the Tasmanian devil – promises to show how the tumours develop and respond to environmental pressures. It seems that the ability of genetically diverse dogs to interbreed has rendered CTVT relatively harmless, by creating the conditions that force its mutations in certain directions and minimise the proliferation of truly dangerous forms. The Tasmanian devil, on the other hand, lives in relative isolation, genetically speaking. Its facial tumour hasn’t been forced to adapt, and it is quickly wiping out the host species.

The mutations of the canine tumour do more than alter how fast its cells replicate. They also allow it to evade detection by a dog’s immune system. That is the only way it can survive for long enough to get passed on. Understand how all this happened, and we might get some clues to the differences between aggressive cancers and unthreatening tumours, allowing us to improve our diagnosis and treatment options for human tumours.

We already know that some mutations which lead to pre-cancerous tumours in the breast and prostate can be less problematic than the results of our aggressive and sometimes unnecessary treatments. Now, thanks to an old dog teaching us new tricks, we might learn why.

Stock photo: Getty Images.

Michael Brooks holds a PhD in quantum physics. His most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

This article appears in the 05 February 2014 issue of the New Statesman, Cameron the captive

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