Nick Carne
Human skin is a battlefield for mutated cells and their clones – and that is a great advantage to us, according to British cancer specialists.
Very few of these cells go on to form cancer because only the fittest survive these epidermal wars – a form of natural selection.
Despite such evolutionary struggles taking place upon it, skin continues to function normally – though we shouldn’t get complacent, warn the specialists, led by Kasumi Murai from the Wellcome Sanger Institute in the UK.{%recommended 1736%}
In a study published in the journal Cell Stem Cell, Murai and colleagues from Wellcome and others from the MRC Cancer Unit at the University of Cambridge used mice to model the mutated cells seen in human skin, focussing on the p53 gene, a key driver in non-melanoma skin cancers.
They created a genetic “switch” that replaced the existing p53 with a gene identical except for a single changed nucleotide (or “letter”). This altered the p53 protein and gave the resulting mutant cells an advantage over their neighbours.
The mutated cells grew rapidly, spread and took over the skin tissue, which became thicker in appearance. However, after six months the skin returned to normal and there was no visual difference between normal and mutant skin.
There are two main types of non-melanoma skin cancer in humans: basal cell, the more common, and squamous cell, which is generally faster growing. Both develop in areas of the skin that have been exposed to the sun.
“The reason that people get non-melanoma skin cancer is because so much of their skin has been colonised by competing mutant cells over time,” says senior author Ben Hall.
“This study shows that the more we are exposed to sunlight, the more it drives new mutations and competition in our skin. Eventually the surviving mutation may evolve into a cancer.”
