Skin cancer rates are rocketing. Thanks to over-enthusiastic sunbathing in previous decades, melanoma cases have tripled in numbers in the UK since the early 1990s – and scientists predict worse is to come. The type of cancer once relatively rare in Britain is now its fifth most common. Broadcaster Chris Evans recently revealed he had been diagnosed with the disease. Scientists say skin cancer is likely to continue to rise up the nation’s tumour prevalence charts: most recent estimates suggest cases will increase a further 50% in the next 20 years. The impact has been particularly marked among adults aged 55 and over. Case rates in this age group have increased by 195% since the 1990s, according to the latest figures from Cancer Research UK. A grim price is being paid for those cheap package holidays and tanned skins that were enjoyed in the 60s and 70s. Early diagnoses and treatments for skin cancer are keeping down deaths but scientists say it is becoming urgent that new therapies are developed, particularly techniques for neutralising melanomas that have metastasized and spread from a patient’s skin to other parts of their body. “We are making progress but we are still not yet at the stage where we have a cure,” said cell biologist Prof Dot Bennett of the Molecular and Clinical Sciences Research Institute, St George’s, University of London. “However, we recently uncovered a very promising process which we hope could become an effective way of dealing with metastatic skin cancer.” The new technique has evolved the creation of a chemical – called a cell-penetrating peptide – that can kill melanoma cells efficiently and selectively, while having few toxic side effects. “We were very surprised at its effectiveness and although a great deal of extra work needs to be done before we can think of using this on human patients, it is very encouraging.” Melanomas are linked to skin cell division. Sometimes, after a single mutation, this can produce moles. “However, after a certain number of divisions, a defence mechanism called cell senescence halts this process and the mole’s growth halts,” added Bennett. “So you can think of a mole as an aborted cancer. If it had not been terminated it would have grown and spread.” The problem is that on occasions further mutations occur in a cell and the process of shutting down its division stops working. The result is melanoma and crucially all of the mutations involved can be triggered by ultraviolet (UV) radiation. The sun is a key source of UV radiation and bathing in its rays without proper protection not only produces sunburnt skin, it can trigger a melanoma that can take many years to materialise. In many cases surgery or radiotherapy can halt the disease. However, in some cases skin cancer can metastasize and spread to other organs before it is spotted. It is this form that has been the focus of research by Bennett and her team. Jointly funded by Cancer Research UK and the British Skin Foundation, they have identified worked on a protein known as p16, which was already known to be able to suppress tumour development, and on a small active part of p16 called a peptide. “We made a series of changes to the peptide that previous research by other scientists showed might be effective and would allow it to enter cells, then added the peptide to melanoma cell lines in the laboratory,” Bennett said last week. “The results were surprising. We expected the peptide might stop the cancer cells dividing. In fact it killed them. Moreover it did not kill normal cells. This deadly impact is important. Like many other cancers, the stage at which melanoma is identified is crucial to a patient’s prospects of survival. The earlier the diagnosis, the better the outcome, as Michelle Mitchell, chief executive of Cancer Research UK, told the Observer. She said: “More people than ever are surviving melanoma skin cancer, but there remains a critical gap in survival between people diagnosed at early stages compared with those diagnosed later. The p16-related peptide offers a promising new approach for those patients diagnosed with metastatic disease.” Adil Sheraz, of the British Skin Foundation, said:. “The protein p16-related peptide preferentially targets melanoma cells, preserving fibroblasts – which play a vital part in skin repair and regeneration – and causing minimal damage to other cells. While further research is needed, this has the potential for much more favourable outcomes for melanoma patients.” Bennett added: “We tried the p16 peptide on three lines made up of metastatic melanoma cells. All of those were nicely wiped out, which is very promising. Obviously we have to do a lot more research before using this technique on humans and that will take several years but it is a very good start.”