Cutaneous melanoma patients have normal repair kinetics of ultraviolet-induced DNA repair in skin in situ.
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'Eclairage 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.
Xu
G
G
Department of Biosciences, Karolinska Institute, Huddinge, Sweden. Guogang.xu@csb.ki.se
Snellman
E
E
Bykov
V J
VJ
Jansen
C T
CT
Hemminki
K
K
D000328:Adult; D004260:DNA Repair / Q000528:radiation effects*; D005260:Female; D006801:Humans; D008297:Male; D008545:Melanoma / Q000235:genetics*; D008875:Middle Aged; D011740:Pyrimidine Dimers / Q000378:metabolism; D012867:Skin / Q000737:chemistry / Q000528:radiation effects*; D012878:Skin Neoplasms / Q000235:genetics*; D013997:Time Factors; D014466:Ultraviolet Rays
D011740:Pyrimidine Dimers