1. Department of Biosciences, Karolinska Institute, Huddinge, Sweden
2. ^*Department of Dermatology, Päijät-Häme Central Hospital, Lahti, Finland
3. ^†Department of Dermatology, University of Turku, Turku, Finland

Correspondence: Dr Guogang Xu, Department of Biosciences, Karolinska Institute, S-14157 Huddinge, Sweden. Email: Guogang.xu@csb.ki.se

Received 30 June 1999; Revised 10 December 1999; Accepted 18 January 2000.

Abstract

The DNA lesions induced by ultraviolet radiation include cyclobutane pyrimidine dimers and 6–4 photoproducts. We investigated whether cutaneous melanoma patients have an impaired ability to repair their ultraviolet-induced photolesions. Seventeen patients with melanoma and 13 healthy controls took part in this study. Both groups received a dose of 40 mJ per cm² Commission Internationale de l'Éclairage of solar simulating radiation on previously unexposed buttock skin. Skin biopsies were taken at 0 h, 24 h, and 48 h after ultraviolet exposure. A ³²P-postlabeling method was used to measure both cyclobutane pyrimidine dimers and 6–4 photoproducts in skin. Cyclobutane pyrimidine dimers and 6–4 photoproduct levels did not differ in the melanoma patients from those in the control group at any time point post-ultraviolet radiation. The repair rate of cyclobutane dimer TT=C was faster than that for TT=T both at 24 h and 48 h postirradiation in both groups, providing evidence of site-specific repair (p < 0.05). We conclude that patients with melanoma have a normal ultraviolet-induced DNA repair capacity in skin in situ.