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ThreatenedA contagious cancer has wiped out about 70 percent of the population of Tasmanian devils (one shown). A new study has pinpointed the cancer's origin.Image courtesy of Anaspides Photography, Iain D. Williams

Scientists have discovered the true identity of a contagious form of cancer that is killing Tasmanian devils. The cancer, called devil facial tumor disease, stems from cells that normally insulate nerve fibers, a new study shows.

Genetic analysis of tumors taken from infected devils in different parts of Tasmania reveals that these insulating cells, known as Schwann cells, became cancerous in a single Tasmanian devil and have since passed to other devils, an international group of researchers reports in the Jan. 1 Science.

Previously, scientists had suspected that a virus might be the source of the infection, but the new study confirms that cancer cells themselves are transmitted from devil to devil.

Knowing the origin of the contagious tumors could help conservationists diagnose the disease more accurately and may eventually lead to a vaccine that would target tumor proteins, says Katherine Belov, a geneticist at the University of Sydney who was not involved with the project.

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Hope for treatmentAn infectious cancer, known as Tasmanian devil facial tumor disease, passes cancer cells from animal to animal through bites. Knowing the disease’s origin is a foundation for better diagnosis and perhaps, eventually, a vaccine or other treatment.Image courtesy of Save the Tasmanian Devil Program

A vaccine against the facial tumor disease, “while now pie in the sky, in 10 years might not be,” says Gregory Hannon, a Howard Hughes Medical Institute investigator at Cold Spring Harbor Laboratory on Long Island, N.Y. “Ten years might be enough time” to save the devils from extinction, he says.

About 70 percent of the Tasmanian devil population has disappeared as a result of the disease, and if the current rate of decline continues, devils could become extinct in the wild in 30 to 50 years, says Elizabeth Murchison, now a postdoctoral researcher at the Wellcome Trust Sanger Institute in Hinxton, England. Murchison, a native of Tasmania who grew up seeing devils in the wild, led the project while working in Hannon’s lab at Cold Spring Harbor. “I didn’t want to sit back and let the devils disappear,” she says.

Genetic data about Tasmanian devils has been lacking, says Belov. An effort to decode the species’ genome is underway but is not yet complete. The new study provides the largest genetic data set collected to date for the species.

“It really does move us so much further ahead to have all of this genetic information,” Belov says.

Murchison and her team analyzed patterns of gene and microRNA activity in facial tumors and in healthy tissue. MicroRNAs are small genetic molecules that help regulate the activity of genes.

All of the 25 tumors the team analyzed were genetically identical, indicating that they came from a single source — most likely a devil that lived about 20 years ago.

Researchers characterized microRNA signatures of both tumors and healthy devil tissues. Analyses of these signatures and gene activity patterns indicated that the tumor cells most closely matched Schwann cells, a type of cell that forms a waxy sheath called myelin around nerve fibers. A protein called periaxin, which is normally found only in Schwann cells, is also present in devil facial tumor cells and might be a good diagnostic marker for the disease, the researchers report.

How the cancerous Schwann cells became contagious is still a mystery, though. “Devils are known to be prone to cancers,” Belov says. “I think it was just some sort of freak of nature that allowed this cancer to be stable and transmitted.”

Tasmanian devils are so genetically similar to one another that their immune systems don’t recognize infectious cancer cells from another individual as foreign (SN Online: 1/12/09). Belov hopes to learn whether the infectious cancer cells have also evolved other methods for evading the animals’ immune systems.

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