Professor Austin Burt from the Department of Life Sciences at Imperial College London, who led the research, said: "Our study has revealed that this type of cancer works in a really unexpected way. It raises some really important questions about the progression of other cancers, such as how they repair their own DNA."

The researchers believe that the cancer does not take up new mitochondria with every new host, rather that this functions as an occasional repair mechanism to replace faulty mitochondria. A naturally high rate of genetic mutation in cancers regularly leads to non-functional genes in the CTVT mitochondria, which causes them to lose productivity.

In an earlier study, Imperial's scientists estimated that the earliest CTVT tumour originated from an ancient dog or wolf approximately 10,000 years ago, perhaps when dogs were first domesticated through intensive inbreeding of the more social wolves. Today's results suggest that over this time, the cancer must have evolved the unusual ability to capture mitochondria from its host animal.

The scientists hope their work can be built upon by medical researchers to advance our knowledge of cancer progression in humans and other animal species.

Source: Imperial College London