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a University of
Rostock, Department of Biology, Division of Cellular Pathophysiology,
Universitätsplatz 2, 18051 Rostock, Germany, b University of Rostock, Department of Medicine,
Division of Dermatology, Rostock, Germany, c University of Rostock, Department of Biology,
Division of Zoology, Rostock, Germany
Correspondence to: Dr Papp.
Received 18 August
1998;
Revised version accepted for publication 24 March 1999
Eighteen human congenital melanocytic naevi (CMN) from 17 patients were screened for activating point mutations in the oncogenes N-ras and
CDK4 and for sequence variants
in the MC1R gene by combined RFLP-PCR/SSCP analysis. In addition, all lesions were screened for
deletions and point mutations in the tumour suppressor genes p53 and
p16INK4a
(CDKN2A) by combined multiplex
PCR/SSCP analysis. Positive screening data were specified by sequencing
of the corresponding PCR product. Activating point mutations in the
N-ras gene (nine CAA (Gln) to AAA (Lys) transversions and one CAA (Gln) to CGA (Arg) transition at
codon 61) were detected at high frequency (56%). Furthermore, three
missense mutations (V92M) and two silent mutations (CGA (Arg) to CGG
(Arg), codon 213, exon 6) were found in the
MC1R and
p53 genes, respectively. No
mutations were found in p16 or CDK4. The activated
N-ras oncogene, which is also
found in human cutaneous melanomas, may constitute a potential risk
factor for melanoma formation within CMN.
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