Abstract

The incidence of cutaneous malignant melanoma (MM) is rising tremendously worldwide in white populations. The reasons for the dramatic increase are not entirely known. A number of factors have been linked etiologically with melanoma, including host factors such as skin complexion, hair and eye color, and number of melanocytic nevi and environmental factors such as sunlight exposure and a positive family history of malignant melanoma. The last mentioned risk factor was recognized in 1978 when the groups of Clark and Lynch simultaneously reported an inherited syndrome characterized by atypical moles and melanomas. Clark et al. (1978) termed this syndrome BK mole syndrome, using the initials of his affected families, while Lynch et al. (1978) called it FAMMM (familial atypical multiple mole melanoma) syndrome. The very exciting clinical feature of these families was the finding that in affected individuals, those with atypical or dysplastic nevi, the risk for developing melanoma approached 100%. The atypical nevus therefore was regarded as the putative precursor for MM. In the following years observations on atypical moles in melanoma-prone families were generalized and applied to individuals who had no family history of the tumor. The term dysplastic nevus syndrome (DNS) was first used for this condition by Elder et al. (1980) and is now widely accepted. Since then, however, many epidemiologic studies have demonstrated a significant lower melanoma risk for these individuals compared with the classic BK mole patients. Therefore, it is now commonly accepted that dysplastic nevi are both a risk indicator and possible precursors of malignant melanomas (Elder 1988).KeywordsMelanocytic NevusMelanoma RiskMelanocytic LesionDysplastic NevusSuperficial Spreading MelanomaThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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