"It offers a real hope we will be able to tackle cancer by putting cells into a permanent coma," Thomas Hughes-Hallett, chief executive of the Marie Curie Cancer Care charity, told a news conference.

Dr Colin Goding and his team were studying a gene called Tbx2 which is overactive in melanoma, the most serious type of skin cancer, when they discovered it was linked to a mechanism that repressed senescence. "What really surprised us was that when we inhibited Tbx2 in melanoma cells, they senesced and stopped dividing. This means we have potentially a new way of stopping cancer cells dividing," said Goding.

Cancer develops when certain genes are mutated and cells divide uncontrollably. Goding compared it to an accelerator in a car being jammed on.

Normal, healthy cells know something is wrong -- the accelerator is jammed -- and put on a brake or senescence. But in cancerous cells the brake is missing or switched off.

The scientists inhibited the action of Tbx2 in melanoma cells in culture with a technical trick. They discovered that the senescence mechanism was still there but had been switched off by the Tbx2 gene.

"What we have done is switched it back on," said Goding who reported the findings in the journal Cancer Research.

He now hopes to find out in what proportion of melanoma and other cancer cells senescence can be induced and whether a drug could be developed to activate it in cancer cells.

But he said it could be up to 10 years before any new treatments based on the findings will be available.

"Being able to design drugs that reactivate senescence would be a great boon. The beauty of it is that this natural mechanism would automatically target cells which have the accelerator jammed on -- it would hit cancer cells, not normal cells," Goding added.

About 133,000 new cases of malignant melanoma are diagnosed worldwide each year. Eighty percent are in North America, Europe, Australia and New Zealand, according to the International Agency on Cancer Research in France.