Human skin has evolved a greater resilience to cancer than other tissue types. It is an outcome that makes a certain amount of sense, given that skin is exposed to the additional mutational burden caused by solar radiation. Researchers here investigate some of the mechanisms involved in this cancer resistance, and suggest that the level of mutational damage is high enough that potentially cancerous mutations are continually being outcompeted by other potentially cancerous mutations. It is rare for any one mutant lineage to dominate sufficiently to generate skin cancer. The goal in this sort of investigation is to find something that could potentially serve as the basis for a cancer treatment. While this is fascinating, I don’t immediately see the potential for any practical use of these findings.
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. However, every person who has been exposed to sunlight carries many mutated cells in their skin, and
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