{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T09:23:39Z","timestamp":1792142619691,"version":"4.4.0"},"reference-count":45,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2002,6,12]],"date-time":"2002-06-12T00:00:00Z","timestamp":1023840000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2002,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>Few long\u2010term clinical and histologic data for melanocytic lesions have been available based on the mutation status of families at an increased risk of melanoma. In the current study, the authors describe the clinical and histologic features of dysplastic nevi and melanoma over time in families at an increased risk of melanoma with differing germline mutations in <jats:italic>CDKN2A<\/jats:italic>, <jats:italic>CDK4<\/jats:italic>, or not yet identified genes.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>Thirty\u2010three families with &gt; 2 living members with invasive melanoma were evaluated clinically and followed prospectively for up to 25 years. All the participants were evaluated by the same study team at the Clinical Center of the National Institutes of Health or in local clinics. After informed consent was obtained, family members (<jats:italic>n<\/jats:italic> = 844) were examined and photographed. Blood was obtained for genetic studies; genotyping for <jats:italic>CDKN2A<\/jats:italic> and <jats:italic>CDK4<\/jats:italic> was performed. Sequential photographs of melanocytic lesions were taken as part of the clinical evaluations. When melanocytic lesions were removed, the histology was reviewed. Representative photographs and photomicrographs were selected for six classes of lesions and three mutation groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>All the families were found to have members with dysplastic nevi and melanoma; 17 had mutations in <jats:italic>CDKN2A<\/jats:italic>, 2 had mutations in <jats:italic>CDK4<\/jats:italic>, and 14 had no mutations in either gene identified. The majority of dysplastic nevi either remain stable or regress; few change in a manner that should cause concern for melanoma. With careful surveillance, melanomas can be found early.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>The melanomas and dysplastic nevi that were found to occur in the study families did not appear to vary by the type of mutation identified in the families. Cancer 2002;94:3192\u2013209. \u00a9 2002 American Cancer Society.<\/jats:p><jats:p>DOI 10.1002\/cncr.10605<\/jats:p><\/jats:sec>","DOI":"10.1002\/cncr.10605","type":"journal-article","created":{"date-parts":[[2002,10,6]],"date-time":"2002-10-06T08:29:56Z","timestamp":1033892996000},"page":"3192-3209","source":"Crossref","is-referenced-by-count":123,"title":["A natural history of melanomas and dysplastic nevi"],"prefix":"10.1002","volume":"94","author":[{"given":"Margaret A.","family":"Tucker","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary C.","family":"Fraser","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alisa M.","family":"Goldstein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffery 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