TUMOURS - Face 'suicide virus'

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BBC Tumour cells face 'suicide virus' Laboratory research supports the new treatment A virus which prompts cancer cells to self-destruct while sparing healthy cells has been developed by researchers.

Although it has so far only been tested in a laboratory, they are hopeful that it could one day form the basis of a cancer therapy for many human patients.

The human adeno-associated virus (AAV) works by harnessing a genetic difference between many cancer cells and their healthy equivalents.

The virus, of a type called parvoviruses, can enter human cells but does not apparently cause any harm itself.

Out of control

The p53 gene, known to cancer researchers for a decade, is thought to be one of the reasons why cancer cells grow out of control and form large, chaotic, tumour shapes.

Its job is to help control the system which either allows the replication - or ensures the destruction - of healthy and damaged cells respectively.

Some sorts of cancer appear to have the ability to stop p53 doing this job properly, which allows malignant cells to divide without restriction.

If tumours from about half of all human cancers are analysed, this altered form of p53 can be found.

It is these patients that the research team, from the Swiss Institute for Cancer Research, are hoping to help.

Their work is reported in the journal Nature.

Their virus prompts a remarkable response when it enters a cancer cell which has an altered p53 gene.

Somehow, the virus kick-starts the mechanism which tells the cell to self-destruct.

However, when the virus goes into a healthy cell, a completely different thing happens - the p53 gene simply held up cell division until the virus had degraded, with no apparent long-term consequences.

In theory, this could help doctors precisely target cancer cells without damaging healthy tissue, as is the case in much chemotherapy and radiotherapy.

The only flaw with the current virus is that it is inactivated, meaning it cannot infect the body cell by cell in the same way as a normal virus, so a similar but live virus may have to be found.

Shrinking tumours

When laboratory mice were given the virus, their tumours all shrank, but there is still likely to be a long delay before human trials can begin.

The institute's team is led by Professor Peter Beard, who said: "No cancer patient should expect any of these innovative approaches to cure them in the near future.

"Continued research into the structure of p53, the proteins to which it binds, and the pathways that it controls should eventually lead to the maturation of one or more of these strategies - each of which has the potential to benefit millions."

-- Anonymous, August 29, 2001


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