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The overwhelming predominance of ultraviolet (UV)-signature mutations in skin cancers reflects the very prominent role of UV-induced (primarily UVB-induced) DNA damage in causing these cancers. UVB-induced damage is typically characterized by cytosine-to-thymine (C-to-T) transitions that occur after repair of cyclobutane pyrimidine dimers (CPDs). Although UVA constitutes >95% of terrestrial UV radiation, its role has been less often studied, and it does not involve C-to-T transitions. Studies suggest that melanin, which is protective against sunburn, DNA damage, and skin cancer, may contradictorily also have carcinogenic effects through reactive oxygen species (ROS) generation. These authors propose a novel pathway in mutagenesis involving …