Wednesday, April 14, 2010

The nerve of one animal

A cancer that spreads from one animal to another has wiped out 
about 70 percent of the population of Tasmanian devils (one shown).
A cancer that spreads from one animal to another has wiped out about 70 percent of the population of Tasmanian devils (one shown).
Image courtesy of Anaspides Photography, Iain D. Williams
A vicious cancer has wiped out 70 percent of the world’s population of wild Tasmanian devils, and if nothing changes, these animals might be extinct in the wild in 30 to 50 years. But there may be hope: In a new study, scientists have identified the cancer and can point to where it starts.
The scientist who led the study is Elizabeth Murchison, who grew up seeing these animals in the wild. “I didn’t want to sit back and let the devils disappear,” she told Science News.
Murchison, who now works at the Wellcome Trust Sanger Institute in Hinxton, England, comes from Tasmania, an Australian island that is the only native home to Tasmanian devils. These animals, which look like small bears, weigh up to 26 pounds, have a long and bushy tail, and often feed on dead animals.
Since 1996, they have been plagued by devil facial tumor disease, or DFTD. As its name suggests, this disease causes large tumors to grow on an infected devil’s face, especially around the mouth. (Devils often bite each other on the face when they meet.) Eventually, the tumors get so large they interfere with eating, and the animal dies of starvation.
To make matters worse, the cancer is contagious. It’s so contagious that some scientists used to believe a virus caused the disease. But that’s not the case — scientists have found that the cancer grows deep in the cells of the central nervous system, and the cancer cells themselves spread from animal to animal through bites (although scientists still don’t know why).
Now that they know where the disease comes from, however, scientists might be able to develop a vaccine that kills the cancer before it becomes deadly, says Katherine Belov. She is a scientist at the University of Sydney, in Australia, who was not involved with the project.
In the study, Murchison and her team reported that the tumors start in cells, called Schwann cells, that usually surround nerve fibers. Nerve fibers, or axons, act like electrical lines in the body: They carry electrical impulses from one neuron (also known as a nerve cell) to the next, or from neurons to muscles.
When the brain sends a signal through the body, the signal travels by way of nerve fibers. Schwann cells wrap themselves around nerve fibers forming a white, wispy layer called myelin. The layer of myelin helps electrical messages zip from one nerve cell to another without shorting out, much like insulation around electrical wires. When a Tasmanian devil’s Schwann cells become cancerous, the animal starts to grow tumors — and becomes contagious.
To understand the cancer, Murchison studied both healthy cells and tumor cells in the animals. In particular, she looked at the genes in the cells. A gene is like a set of instructions for how to build proteins, which are key ingredients that make our bodies work. All the genes together of an organism are called its genome — and a genome is a like a complicated recipe which in humans has more than 20,000 sets of instructions to create its key ingredients.
In a healthy cell, all the genes are working properly. But in a cancer cell, some of the genes aren’t working. Some genes might be “silenced,” or turned off, like a light switch — so they’re not doing their jobs. And other genes might be doing too much of their job — and making too much of one ingredient. (Think about a recipe with too much salt.)
In addition to comparing the genes of healthy and cancerous cells, Murchison looked at microRNAs, which are tiny pieces of genetic material in a cell that help determine which genes get turned on and off. She and her team studied 25 tumors and found they had the same genome (or were “genetically identical”). This led the scientists to conclude that the disease started in a single Tasmanian devil that probably got sick about 20 years ago.
She and her team also noticed that the patterns of genetic activity in the tumor cells (that is, the genetic instructions the cells were following) looked like the patterns found in Schwann cells — which led the scientists to conclude that Schwann cells were the source.
Gregory Hannon, a scientist at Cold Spring Harbor Laboratory on Long Island, N.Y., who worked with Murchison, says that right now, a vaccine that will save the Tasmanian devils is probably a long way off. But that may change in a decade. “Ten years might be enough time” to save the animals, he told Science News.

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