Slip off a shirt, slop on some DNA
The risk of skin cancer is clearly linked to UV exposure. This risk is significantly heightened in individuals with such diseases as the rare human disorder xeroderma pigmentosum (XP), which is caused by mutations in genes encoding components of the DNA repair pathways. Now, Gilchrest and colleagues demonstrate that pre-treating wild-type or partially repair-deficient XP+/− heterozygous nude mice with DNA oligonucleotides enhances DNA repair capacity, decreases mutation frequency and reduces and delays carcinogenesis after UV irradiation. Building on the observation that thymidine dinucleotides (pTT) trigger a protective response in cells after exposure to UV radiation, the authors apply a 'sunscreen' consisting of pTT oligonucleotides in a lotion to mice, followed by a regime of UV exposure lasting up to 24 weeks. Wild-type mice were found to be free from neoplasms for 7 weeks longer than controls, and pTT-treated XP heterozygotes displayed 50% fewer neoplasms at 24 weeks than did control mice. This approach may provide an advantage for fighting skin cancer in high-risk individuals and could also become a general formulation for sunscreen. (Proc. Natl. Acad. Sci. USA 101, 3933–3938, 2004) NC
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