Normal skin contains a patchwork of mutated cells, yet very few go on to eventually form cancer and scientists have now uncovered the reason why. Researchers at the Wellcome Sanger Institute and MRC Cancer Unit, University of Cambridge genetically engineered mice to show that mutant cells in skin tissue compete with each other, with only the fittest surviving. The results, published today (27 September) in Cell Stem Cell suggest that normal skin in humans is more resilient to cancer than previously thought and can still function while a battle between mutated cells takes place in the tissue.
Non-melanoma skin cancer in humans includes two main types: basal cell skin cancer and squamous cell skin cancer, both of which develop in areas of the skin that have been exposed to the sun. Basal cell skin cancer is the most common type of skin cancer, whereas squamous cell skin cancer is generally faster growing. There are over 140,000 new cases of non-melanoma skin cancer each year in the UK*.
However, every person who has been exposed to sunlight carries many mutated cells in their skin, and only very few of these may develop into tumours. The reasons for this are not well understood.
For the first time, researchers have shown that mutated cells in the skin grow to form clones that compete against each other. Many mutant clones are lost from the tissue in this competition, which resembles the selection of species that occurs in evolution. Meanwhile, the skin tissue is resilient and functions normally while being taken over by competing mutant cells.
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