Virus that improves anti-cancer drugs' efficacy unveiled

London, November 7 : A Canadian researcher team says that the efficacy of anti-cancer drugs in destroying tumours, or in keeping them in check, may be improved with the aid of a virus called reovirus.

Brad Thompson, CEO of Canadian company Oncolytics Biotech that has been developing the virus as a product called Reolysin, has revealed that this virus harmlessly infects most people at some time in their lives.

He says that the reovirus destroys tumour cells because they lack the cellular machinery that keeps the virus in check in healthy cells.

His proposition is based on two recent studies wherein patients with head and neck cancer were injected with the virus alongside anti-cancer drugs.

The research showed that cancers either stopped growing or shrank in almost all recipients with the addition of the virus to anti-cancer therapy.

It was also observed that the patients had cancers that had become resistant to all existing therapies.

"Some patients had very aggressive tumour shrinkage of as much as 95 per cent," New Scientist magazine quoted Thompson as saying.

One of the trials was conducted at the Royal Marsden Hospital in London, led by Kevin Harington.

The researchers involved noticed that eight out of nine patients responded positively after the virus plus two standard anti-cancer drugs, paclitaxel and carboplatin, had been infused into their bloodstream. In four patients tumours stopped growing, while they shrank dramatically in another four.

In the other trial, also near London at the Royal Surrey Hospital, nine out of 11 patients responded well after receiving the virus plus the anti-cancer drug docetaxel.

While the results of the study suggested that the virus could actually help in some way, Thompson said: "Usually, only 10% of patients respond when the cancer comes back and they're having their second course of treatment."

The researcher revealed that the virus attacks cancerous cells with genetic defects, which means that a gene called Ras, which directs the cell to multiply, is permanently switched on, making the tumour grow continuously.

Thompson highlighted the fact that such defects in the Ras gene are seen about two-thirds of primary cancers, and 90 per cent of secondaries.

However, some experts are of the view that it is too early to tell whether it's the drugs or the virus, or the combination, that's making the difference.

"It is likely that some patients would show a response to the chemotherapy alone. However, it's encouraging to see quite striking responses in this group who have difficult tumours to treat, and we will look forward to seeing the results of further trials in the future," says Peter Johnson of the University of Southampton.

Thompson says the criticism is completely valid, but insists that a recent trial of Reolysin alone in patients with soft-tissue sarcoma (a cancer with no cure at all) showed that the cancer stabilised in a fifth of the patients.

So far, about 240 patients have been treated in 12 trials around the world-some in combination with other drugs, some in combination with radiation therapy, and some with Reolysin alone.

The only side-effects of the therapy involving the virus have been mild fevers, transitory aches, and pains in joints and muscles.

The researchers say that they may be able to confirm the efficacy of their novel approach upon the completion of a much bigger trial in the UK, involving 200-300 head and neck cancer patients.

The findings were presented at the International Society for Biological Therapy of Cancer annual meeting in San Diego, California, which finished 2 November.

ANI