Cutaneous melanoma patients have normal repair kinetics of ultraviolet-induced DNA repair in skin in situ

被引:33
作者
Xu, GG [1 ]
Snellman, E
Bykov, VJ
Jansen, CT
Hemminki, K
机构
[1] Karolinska Inst, Dept Biosci, S-14175 Huddinge, Sweden
[2] Paijat Hame Cent Hosp, Dept Dermatol, Lahti, Finland
[3] Univ Turku, Dept Dermatol, Turku, Finland
关键词
photoproduct; P-32-postlabeling; DNA repair; case-controls;
D O I
10.1046/j.1523-1747.2000.00943.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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 cm(2) 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 P-32-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.
引用
收藏
页码:628 / 631
页数:4
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