The incidence of melanoma continues to rise in most fair‐skinned populations around the world. This year, 68,720 Americans will be diagnosed with melanoma and more than 8,500 will die from the disease, an enormous toll for a largely preventable cancer. Strategies to control the burden of melanoma include primary prevention, early detection of treatable lesions, and novel therapies for established disease.

Primary prevention requires understanding of the modifiable causal factors, and then developing programs to intervene at the population level to reduce the incidence of new cases. To date, the only modifiable factor yet identified is solar ultraviolet radiation (UVR). Somewhat unusually in cancer research, the most compelling human data for a causal association between sunlight and melanoma come from ecological studies comparing the incidence of melanoma across populations, over time, and following migration. Animal models are limited in number, but mostly confirm that exposure to UVR, particularly early in life, causes melanoma. Data regarding the role of solar UVR from observational epidemiological studies is abundant but inconsistent, and data from intervention trials is almost non‐existent. Thus the evidence‐base with which to enact primary prevention policies for melanoma is limited. Moreover, recent epidemiologic and molecular findings indicating that melanomas arise through multiple causal pathways pose interesting new challenges for designing primary prevention interventions. Early detection is another approach to reducing the melanoma burden. The strategy to identify and remove threatening melanocytic lesions before harm ensues is widely practiced, although nowhere is this done systematically across entire populations. Several considerations have precluded the formal introduction of melanoma screening programs, particularly the low predictive value of current screening methods and the consequent costs of overdiagnosis of pigmented lesions. Research to improve screening performance, including the identification of high‐risk populations using phenotypic and genotypic markers, is currently underway and may lead to new approaches.

The final pillar of melanoma control lies in finding better treatments, especially for disseminated melanoma which has proven to be largely resistant to ‘traditional’ cancer therapies. Research into the mutations occurring within melanoma tumors is anticipated to identify novel targets for treatments, as well as lead to better understanding of the causes of melanoma. Limited success has been made with c‐Kit; it is hoped that other targets will follow from molecular characterization of these tumors.

This presentation will introduce these concepts, aspects of which will be addressed in more detail by the panel speakers with respect to both melanoma and keratinocyte cancers.

Citation Information: Cancer Prev Res 2010;3(1 Suppl):CN12-02.