Cancer find touted worldwide

Cancer researchers at the UCalgary's Faculty of Medicine have discovered a naturally occurring human virus that kills cancer cells, a discovery that may one day provide new therapies for cancer patients.

Announced at a jammed press conference Nov. 12 at Heritage Medical Research Building, the news quickly made national and international headlines.

The virus — called reovirus (reo is an acronym for respiratory enteric orphan) — is a naturally occurring virus believed to cause mild infections of the upper respiratory and gastrointestinal tract of humans. The UCalgary researchers found that reovirus is a potent killer of cancer cells whose growth signal has gone awry.

A major biochemical pathway that controls cell growth is the Ras signalling pathway. In cancer cells, this pathway is highly activated, resulting in unrestricted cell growth. Activation of this pathway could be due to mutations in the Ras gene itself, or mutations in the elements upstream or downstream of Ras in the pathway.

The UCalgary team — virologist and cancer biologist Patrick Lee (above), graduate student Matthew Coffey, and Lee's colleagues James Strong and Peter Forsyth — recently discovered that reovirus selectively kills cells with an activated Ras pathway. Infection of a single cancer cell by a single reovirus particle can generate a thousand progeny reovirus particles, which in turn infect neighbouring cancer cells. This cycle continues until all cancer cells are eliminated. Normal cells are spared.

These results are beyond our wildest dreams... Based on the reovirus infection mechanism we have revealed, the more malignant the tumour, the more effective reovirus is in killing it. It's like the reovirus is saying: `If you're bad, you're the first to go.

Patrick Lee

In a report published in the Nov. 13 issue of Science, one of the top two scientific journals in the world, Lee and his team used reovirus to treat both mouse tumours and human brain tumours (glioblastomas) implanted in mice.

In tumours implanted in mice lacking an immune system, a single injection of reovirus directly into the tumour was sufficient to shrink the tumour. In mice with a competent immune system, multiple injections were required. Reovirus treatment was effective even in mice that had previous exposure to reovirus, and thus had circulating antireovirus antibodies in their bodies. Tumours that completely regressed have not reoccured during the four months after the cessation of the treatment.

As a benign virus with the ability to destroy cancer cells, reovirus is expected to be an important anticancer therapeutic.

Lee and his colleagues have submitted an application to Canada's Health Protection Branch for Phase I clinical trial using reovirus.

The study leading to this discovery was funded by the Medical Research Council of Canada, the Alberta Cancer Board, and the Alberta Heritage Foundation for Medical Research. The infrastructure was provided by TransCanada Pipelines Ltd. through its donation to the Partners in Health Campaign.

Lee and his coworkers are part of UCalgary's Cancer Biology Research Group in the Faculty of Medicine. His team also recently discovered a link between DNA damage and cancer development.