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By HELEN BRANSWELL
For the past decade or so, cancer researchers have been studying how viral therapy - the use of common viruses such as the herpes simplex virus could be used to destroy cancer cells while keeping healthy cells intact.
But while scientists are coming to the conclusion that the technique can work, they haven't exactly known why. Until now.
A research team from the University of Calgary has determined what happens in the herpes virus that allows it to become a potent cancer fighter. The discovery, suggests lead author Patrick Lee, will speed research into viral therapies for cancers.
"We have learned a very important lesson from this work - how to make a normal virus into a cancer-killing virus," Lee, an expert in cancer biology said in an interview from Calgary
The article on the findings was published in the journal Nature Cell Biology
Dr Robert Martuza, who is currently conducting human trials on the use of the herpes virus as a cancer therapy says Lee's findings will help researchers design personalized cancer treatments, possibly within the next year or two.
Lee is already quite well-known for his work on the reovirus, a naturally occurring bug that poses no threat to humans yet can destroy cancer cells with stunning accuracy
Still, his findings on the workings of the herpes virus are likely to raise eyebrows.
"I'm not a herpes person... ," he said with a laugh. "The herpes virus and the reovirus, they are very different viruses. It's like comparing apples and oranges."
But they are both fruit And Lee was curious to see whether other viruses worked the way the reovirus works when it comes to cancer fighting.
What he found was that the initial barrier the two viruses must overcome once inside a cell happens to be the same.
At the heart of the process is something called the Ras signaling pathway which regulates cell growth. The Ras pathway is a series of cascading biochemical events, not unlike a tumbling chain of dominoes. The first domino falls, knocking down the next, and eventually the final domino falls into the nucleus - the command centre - of a cell and starts telling it what to do.
In healthy cells, the Ras pathway is not very active. It's also finely regulated; the dominos don't begin to fall until they get a signal to do so.
But in cancer cells, some genetic mutation causes the process to become hyperactive.
It turns out the herpes virus needs that hyperactive Ras pathway to spread. That's because the herpes virus being used to fight cancer has been genetically modified so that it can't infect the person getting the treatment.
Since the herpes virus's own cancer-fighting tools have been taken away - when scientists engineered it to make it harmless to healthy cells - it has to rely solely on the tools of the Ras pathway Because it has only one set of tools at its disposal, those tools have to be powerful ones.
As a result, it is drawn to cancer cells and shuns healthy cells.
"If the chain is only active some of the time the virus doesn't like it. The virus will even die," Lee said. "By reducing its risk to human health, you actually enhance its cancer-killing potential."
Calgary � Canadian Press THE KITCHENER RECORD July 2001