"The first time your skin is damaged by sunlight most cells are able to repair the damage and if not they self destruct." The p53 gene is in control, so the skin recovers or undergoes apoptosis, recognisable as the pink sunburn which adds colour to British bodies on beaches around the world So it seems that unsightly peeling is good for us. Professor Brash's theory explains how repeated exposure to UV light causes skin cancer."You can think of it in terms of three trips to the beach," he says. But then with a bad referee, all hell can break loose on the football pitch.Over the past 10 years, scientists have found mutations in the p53 gene in many of the most common cancers including breast cancer and colorectal cancers. In Nature, last month, Douglas Brash, Professor of Genetics at Yale University School of Medicine in Connecticut, and his team reported that they had analysed 45 samples of pre-cancerous skin and discovered that nearly two-thirds had mutations in their p53 genes, indicating that such alterations are an early event in the development of skin cancer.Skin cancer is increasing because more UV light is reaching us through the thinning ozone layer and people are sunbathing more. Putting the cell on hold while DNA is mended, has earned p53 the title "guardian of the genome". For initiating cell death it has also, more recently, been dubbe d "guardian of the tissue."Mutations in DNA are routinely corrected by p53's swift action, but if the mutation occurs in the p53 gene itself, then this can lead to cancer. p53 can trigger the cell to commit suicide, although scientists do not fully understand what dictates the suicide or repair option.

This process, called apoptosis, removes damaged cells in a carefully controlled manner analogous to sending a player off the pitch. They found that p53 doesn't just slow down cell growth, it also directly stimulates the DNA repair machinery via a second gene, known as GADD45 (growth-arrest-and-DNA-damage-inducible).In some cases the cell adopts a more severe strategy to deal with damage. Some of the support genes have recently been identified.At the end of last year, a group of American researchers led by Albert Fornace, Professor of Molecular Biology at the National Cancer Institute in Maryland, claimed to have found the cell's equivalent of the trainer who brings on the magic sponge to put an injured player back in the game. By policing the cell, it suppresses the development of tumours. When the DNA is damaged, p53 - acting as the referee - temporarily halts the normal cycle of cell growth and development, allowing time for patrolling teams of enzymes to repair the damage.In its pivotal role, p53 regulates the actions of many other supporting genes, in the same way as a referee can call on the trainers from the bench.

The overall effect is to slow the game down and ensure fair play and minimal disruption.Dr David Lane from the Cancer Research Campaign Laboratories at the University of Dundee first proposed that p53 can perform a similar role in the cell to avoid permanent damage two years ago. A referee can blow his whistle and stop the game when he spots a foul. Then he may allow a trainer on to the pitch to treat an injured player; or he may send a man off if his behaviour is unacceptable. "If cells divide when they are abnormal, the chances of getting cancer are much greater," says Professor MacKie.One gene in particular, called p53, plays a crucial role in controlling the performance of many cells in our body in much the same way that a referee controls a football match. Specialised enzymes can cut out the fused units and replace them with normal ones.

These enzymes were last month named "Molecules of the year" by the American journal Science.It is vital that defective DNA is repaired quickly before a faulty copy is made. Fortunately, a cell has all the necessary equipment to correct the damage. Most frequently sunlight welds together two of the millions of sub-units that make up the molecule of heredity. This prevents DNA from being copied normally, just as the instructions of a manualwould be misread if two pages were stuck together. All forms are on the increase, but the biggest increase has been in cases of malignant melanoma. "The numbers of malignant melanoma have doubled in the past 10 years," says Professor MacKie.But there is hope: scientists are making progress in understanding how cells deal with the perpetual risk of damage from the Sun's ultraviolet light and how the failure of these processes can lead to melanoma.Exposure to UV light (or some toxic chemicals) damages DNA.