Hard-bitten. When Tasmanian devils bite each other, they can spread a fatal cancer.

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Origin of Tasmanian Devil Tumors Identified

Tasmanian devils may be fierce, but they're no match for a contagious cancer that is decimating their population. Scientists have now identified the type of cell that gave rise to these tumors--a discovery that may spur development of a test or vaccine for the lethal disease.

The stocky, black-and-white Tasmanian devil is an Australian carnivore related to kangaroos and koalas. In the mid-1990s, researchers began to notice that animals were dying from what became known as devil facial tumor disease (DFTD), a cancer that produces disfiguring growths on the head and kills within a few months. According to some predictions, DFTD could wipe out wild Tasmanian devils in less than 40 years.

DFTD is unusual because it spreads from animal to animal but not via a virus, like some human cancers. Instead, the devils appear to spread the cancer cells themselves, mainly through biting. The rogue cells then settle down in their new host and grow into tumors. But the cell type that gave rise to the cancer has been a mystery.

To delve into the cancer's genealogy, molecular biologist Elizabeth Murchison of the Wellcome Trust Sanger Institute in the United Kingdom and colleagues used a technique called deep sequencing. Their approach involved analyzing microRNAs--small strands of RNA that help control gene activity--from healthy tissue and DFTD growths. Each type of tissue in the body normally shows a characteristic pattern of miRNA production, and the team found that devil tumors clustered with samples from the nervous system.

The researchers further narrowed DFTD's origins by determining which genes were switched on in normal and cancerous devil cells. In their gene-activity profile, tumors were most similar to the Schwann cells that insulate nerves outside of the brain and spinal cord by secreting a fatty substance known as myelin. For instance, the tumors manufacture the distinctive Schwann cell protein periaxin, which is part of the myelin-making biochemical pathway. The researchers reported in last week's issue of Science that DFTD probably first began when a Schwann cell or one of its less-specialized precursor cells became cancerous.

Tasmanian devils are prone to a variety of tumors, and the results might lead to methods for quickly distinguishing animals with DFTD, says Murchison. "We found specific genes that allow us to tell the difference between this transmissible cancer and other kinds of cancer in devils." She and her colleagues suggest a diagnostic test that screens for periaxin. Another possible benefit is a vaccine that spurs the devil immune system to eliminate DFTD cells--something it apparently fails to do.

"It's a nice piece of work," says viral oncologist Robin Weiss of University College London. By revealing which genes are active in tumors, the study might also provide clues about how the cancer cells survive and why they can jump from animal to animal, says disease ecologist Hamish McCallum of the Griffith School of Environment in Australia. At the same time, says McCallum, the findings raise a question: "This is clearly a trick that cancer can play, so why is it so rare?"