作者: Christine E. Belgaid , Jonathan L. Rees , Eugene Healy , Ishtiaq Rehman , Minoru Takata
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摘要: A multistep genetic model of tumorigenesis, based on alterations in benign and primary malignant lesions, has been proposed for neoplasms such as colonic carcinoma. However, evidence a similar progression melanoma relied heavily findings cultured lesions or metastases. We have investigated every autosomal arm loss heterozygosity 41 cutaneous melanomas 32 melanocytic nevi, several chromosome arms that show 27 Spitz nevi (a nevus with histological similarities to melanoma). Loss was identified most frequently chromosomes 9p (46%) at loci near the p16INK4 gene, 10q (31%), 6q 18q (22%); these were related melanoma. Only two (both which showed atypical features histology) demonstrated alterations, including p9 one case. In addition, contained interstitial deletions 9p. Our is not confined melanoma, but other uncultured can also display this arm, changes (e.g., 10q, 6q, 18q) may be important conveying phenotype