BBC Science Correspondent James Wilkinson: Scientists isolated the gene while treating cancer patients in the UK

The discovery could eventually lead to a new drug to treat common types of cancer such as lung, breast and colon cancer and it is expected to greatly increase scientists' knowledge of the way cancer spreads.

The mutated gene, Bcl10, was originally thought to be linked only to a rare form of cancer called B cell non-Hodgkin's lymphoma.

But Dr Martin Dyer of the Institute of Cancer Research and his team identified it in other more common forms.

The gene has been compared with P53, which is abnormal in around 50% of all cancers.

Dr Dyer says he expects mutated Bcl10 could also be present in a large number of cancers, but adds that it is "early days to say whether it will be as important as P53".

Preliminary indications suggest cancer cells with mutated P53 do not also have mutated Bcl10.

This could mean that any drugs developed from research into the two genes could cover a very large number of common cancers.

Professor Peter Garland, chief executive of the Institute of Cancer Research, which supported the research with the Cancer Research Campaign, the Leukaemia Research Fund and the Kay Kendall Leukaemia Fund, said: "This is a remarkable discovery which will have a major impact on the direction of cancer research."

Stomach tumour

The gene was isolated from a sample tumour of a man with B-cell lymphoma of the stomach.

It was found that Bcl10 had prevented the death of cancerous cells in the tumour.

Normal P53 and Bcl10 molecules act as quality control inspectors, preventing cancerous cells from reproducing.

Mutant Bcl10 makes cells cancerous

Analysis showed that mutant forms of Bcl10 not only prevent abnormal cells from dying and speeds up their reproduction - like P53 - but it actively changes cells so they become malignant.

Research into mutant P53, which was identified as being involved in the spread of cancer in the late 1980s, is looking at treatments involving the introduction of normal P53 molecules into cells.

But with Bcl10, Dr Dyer believes it may be easier to develop a treatment, if scientists can find a way of switching off the mechanism which makes cells malignant.

The research, published in Cell magazine, is a coup for British scientists. Research into Bcl10 tends to be dominated by US groups.

Ken Campbell, information officer at the Leukaemia Research Fund, said the findings could be "very, very exciting", particularly if mutated Bcl10 is present in cancers which do not contain mutated P53.

"This will trigger a lot more research," he said.