Where have dysplastic nevi led us?
In 1977, Dr. Mark Greene and Dr. Wallace Clark examined members of the B. and K. families, in which several individuals had developed cutaneous malignant melanoma. They recognized that both families had nevi that were unusual in morphology, pattern, distribution, size, and number. These dysplastic nevi identify the individuals in melanoma-prone families who are at increased risk of melanoma; the cumulative risk of melanoma approaches 100% in affected members. Formal genetic analyses have revealed that the dysplastic nevus and melanoma traits appear to be pleiotropic effects of a single, highly penetrant, autosomal dominant gene. Linkage studies have revealed weak linkage with Rh on the short arm of chromosome 1 (1p), and excluded linkage with the HLA region on chromosome 6p, transferrin on 3q, H-ras on 11p, and Gm on 14q. The most promising location for the melanoma/dysplastic nevus susceptibility locus remains chromosome 1p. Future studies will focus on the localization of the melanoma gene, and then the characterization of the gene product to elucidate the etiology of melanoma.
D002878:Chromosomes, Human, Pair 1; D008040:Genetic Linkage; D006801:Humans; D008545:Melanoma / Q000235:genetics*; D009506:Nevus / Q000235:genetics*; D012307:Risk Factors; D012878:Skin Neoplasms / Q000235:genetics*