Sunlight (ultraviolet radiation) has been identified as the major environme
ntal risk factor for the development of cutaneous malignant melanoma and dy
splastic naevi. This is, however, not sufficient to explain all melanoma ca
ses. In recent years much emphasis has been given to genetic susceptibility
to melanoma. A biomarker of susceptibility to environmentally related canc
er is mutagen sensitivity. This is measured as the number of chromatid brea
ks in lymphocytes which are exposed to bleomycin in the G(2) phase of the c
ell cycle. It has been described that patients with common melanoma show an
increased mutagen sensitivity compared with controls. In the present study
mutagen sensitivity was measured in 10 dysplastic naevus syndrome patients
and compared with that in 11 patients with common melanoma. We found simil
ar results for common melanoma patients as have been reported earlier: a re
latively high mean breaks per cell value (0.93 +/- 0.31). In contrast, mela
noma patients with dysplastic naevi showed a significantly (P<0.01) lower m
utagen sensitivity value (0.46 +/- 0.34). This phenomenon was even more pro
nounced when only hereditary dysplastic naevi patients (one or more family
members with dysplastic naevi) were considered (n=5; 0.24 +/- 0.05). These
results suggest a difference in the initiation of the carcinogenic process
in melanoma with a dysplastic naevus as a precursor and melanoma without dy
splastic naevi. (C) 1999 Lippincott Williams & Wilkins.