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April 13, 1984

Precursors to Malignant Melanoma

JAMA. 1984;251(14):1864-1866. doi:10.1001/jama.1984.03340380046022

The incidence of melanoma and the number of deaths from it are increasing in many areas of the world. There is evidence that early recognition and surgical removal of melanoma make this a highly curable cancer. In recent years, medical scientists have become aware of a possible association between certain preexisting pigmented skin lesions and cutaneous melanoma. This interest has developed from identification of two suspected precursors to cutaneous melanoma: (1) acquired abnormal moles known as dysplastic nevi, present both in the general population and in certain melanoma-prone families, and (2) certain congenital nevi. Identification and appropriate management of such precursors could substantially reduce the incidence of and mortality from melanoma.

In an effort to resolve some of the questions surrounding these issues, the National Institutes of Health convened a Consensus Development Conference on Precursors to Malignant Melanoma on Oct 24 through 26, 1983. After a day and a half of presentation by experts of data on these two types of lesions and their potential for becoming cancerous, a consensus panel that included representatives from dermatology, pathology, oncology, family medicine, immunology, epidemiology, and the general public considered the scientific evidence and agreed on answers to the following key questions:

  1. Can dysplastic nevi and congenital nevi be defined clinically and histologically?

  2. Are these nevi precursors to melanoma? What are the prevalence, natural history, and determinants of these precursors?

  3. What is appropriate management of patients with dysplastic nevi and congenital nevi regarding diagnosis, treatment, follow-up, familial screening, and education?

  4. What directions should be taken for future research on precursor lesions to melanoma?

Conclusions  This conference highlighted an important advance in our understanding of melanoma through the identification of a familial syndrome in which multiple dysplastic nevi are associated with development of melanomas. The investigation of patients with this syndrome affords an opportunity not only to advance our knowledge of the biology of melanoma but also to aid the identification of treatable precursor lesions and early melanomas. The result may be a reduction in mortality in these patients.The consensus panel found that melanoma may arise de novo as well as in association with preexisting melanocytic nevi. The panel also agreed that the dysplastic nevus, a distinctive lesion both clinically and histologically, has been identified in this context, particularly in melanoma-prone families. Dysplastic nevi are both markers and precursors for familial melanoma. Melanoma may develop also in congenital nevi, especially when the lesion is larger than 20 cm.Strategies for treatment and follow-up should be formulated individually, on the basis of the risk of melanoma to each patient. Patients with dysplastic nevi and a family history of melanoma should be followed up frequently, with documentation of lesions and excision of changing nevi. The relatives of patients with melanomas should be examined for dysplastic nevi and melanoma in view of the familial aggregation of both lesions. Patients with congenital nevi should be followed up periodically for changes. Need for education in examination of lesions by patients, relatives, and health professionals is emphasized.The scarcity of existing information on precursors of melanoma coupled with its increasing incidence indicate a continuing need for research. Epidemiologic, clinical, and laboratory studies are required of populations known to be at increased risk for melanoma as well as of general populations. Pilot studies should be initiated to evaluate the feasibility of and methodology for large-scale prospective studies. The feasibility and effectiveness of proposed interventions also should be determined. Laboratory studies should be directed toward understanding how pigment cells in precursor lesions undergo transformation.