Melanoma prevention

UV radiation is the major environmental risk factor for melanoma; protection from exposure is an important primary prevention tool. Skin examinations by physician and patient self-exams are vital secondary prevention tools that stop progression of precursor lesions and early-stage melanomas. Enhancing DNA repair is a promising tactic for reducing UV-related melanoma risk. These strategies/agents require validation in appropriate clinical and preclinical models (Table 3.1). The cholesterol biosynthetic pathway participates in activation of oncogenes, making it a viable target for melanoma prevention despite limitations of epidemiological data supporting the efficacy of statins. These strategies/agents require validation in appropriate clinical and preclinical models (Table 3.1). NSAIDs could have some ability to lower the risk of melanoma. These strategies/agents require validation in appropriate clinical and preclinical models (Table 3.1). Antioxidants, including those derived from dietary agents, have promising activity for reducing UV-induced skin damage and for prevention of melanoma. These strategies/agents require validation in appropriate clinical and preclinical models (Table 3.1). IFN-α reduces phospho-STAT3 in dysplastic nevi, a promising biomarker of melanoma progression.