The New York Times,
January 25, 2011 Link
When humans domesticated dogs at least 10,000 years ago, an apparent side effect was a bizarre new kind of parasite. A canine cancer gained the ability to spread from one dog to the next, creating new tumors along the way.
Today, it thrives in dog populations around the world. Scientists are now studying canine transmissible venereal tumors (or C.T.V.T.) to uncover the adaptations the disease uses to thrive in its peculiar way. In the current issue of Science, British scientists report that it upgrades its energy supply by stealing new parts from its canine hosts.
The Russian scientist M. A. Novinsky first discovered C.T.V.T. in 1876. He found that when he transplanted the tumors from one dog to another, they could take hold and grow. But the idea that cancer cells could travel from one host to another was too strange for many to accept. Some scientists argued that some kind of virus caused C.T.V.T., much like human papillomavirus causes cervical cancer.
In recent years, scientists have begun to study the genes of C.T.V.T. cells, and their results have confirmed that it is indeed an infectious cancer. In the last decade, two teams of scientists -- one based at Imperial College London and another at University College London -- independently gathered samples of C.T.V.T. from dogs around the world. They sequenced snippets of their DNA and discovered the tumors were closely related to tumors in other dogs, not to the healthy cells in the host dogs.
After they analyzed the mutations in different cells, both teams concluded that the tumors descended from an ancestral cancer that existed within the past few centuries. But the Imperial College team also looked further back, to when a healthy cell first turned cancerous. They estimated the transition happened several thousand years ago -- perhaps coinciding with the domestication of dogs.
“It’s an asexual, single-celled mammal, in a sense,” said Austin Burt, a member of the Imperial College team. “We talk about calling it Canis cancer.”
Scientists have discovered only one other case of infectious cancer. Tasmanian devils can become infected by a facial tumor when they bite each other. Researchers have proposed that the Tasmanian devils are vulnerable to the cancers because they have little genetic variability. Tumors may be too similar to a devil’s own cells to be rejected.
When dogs first evolved from wolves, they also had little genetic variation. “There weren’t too many friendly wolves around,” said Clare Rebbeck, a colleague of Dr. Burt’s who has since moved to Cold Spring Harbor Laboratory in New York. Dogs then exploded in numbers and diverged into many different breeds. But C.T.V.T. today can infect them all.
To get a more detailed look at the history of C.T.V.T., Dr. Rebbeck and her colleagues turned their attention to a second source of DNA in the tumors. Every animal cell contains structures called mitochondria that produce the cell’s fuel. Mitochondria also contain a small amount of their own DNA.
When the scientists compared pieces of DNA from the mitochondria, they were surprised to find that some samples were more closely related to genes from healthy dog cells than from other tumors. In other words, the mitochondria in C.T.V.T. cells do not all descend from a common ancestor.
Dr. Burt and his colleagues propose that C.T.V.T. sometimes grab mitochondria from the dogs they infect. They speculate that fresh mitochondria would come in handy, because their own mitochondria would acquire mutations, making them worse at generating fuel. Cells that upgraded their mitochondria could grow faster. “This paper is very interesting and exciting,” said Elizabeth Murchison, a geneticist at the Wellcome Trust Sanger Institute in Britain. Dr. Murchison is currently sequencing the entire C.T.V.T. genome and expects to finish the project later this year.
“I’m curious to see the genome sequence,” Dr. Burt said. He expects many more adaptations will turn up. “How many genes has it been able to get rid of? Brain genes aren’t needed any more.”
Copyright 2011 The New York Times Company. Reprinted with permission.