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Melanoma and nonmelanoma skin cancer chemoprevention: A role for nicotinamide?
Author(s) -
Minocha Rashi,
Damian Diona L.,
Halliday Gary M.
Publication year - 2018
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12328
Subject(s) - pyrimidine dimer , skin cancer , actinic keratoses , dna damage , cancer research , xeroderma pigmentosum , nicotinamide , melanoma , carcinogenesis , dermatology , immunosuppression , medicine , dna repair , niacinamide , reactive oxygen species , chemistry , dna , biology , cancer , immunology , pathology , biochemistry , basal cell , enzyme
Summary Ultraviolet radiation ( UVR ) causes DNA damage in melanocytes by producing photolesions such as cyclobutane pyrimidine dimers and 8‐oxo‐7‐hydrodeoxyguanosine. The production of reactive oxygen species by UVR also induces inflammatory cytokines that, together with the inherent immunosuppressive properties of UVR , propagate carcinogenesis. Nicotinamide (Vitamin B 3 ) enhances DNA repair, modulates the inflammatory environment produced by UVR , and reduces UV ‐induced immunosuppression. As nicotinamide reduces the incidence of actinic keratoses and nonmelanoma skin cancers in high‐risk individuals and enhances repair of DNA damage in melanocytes, it is a promising agent for the chemoprevention of melanoma in high‐risk populations.