DOI: 10.1158/1055-9965.epi-08-0248. Repair of UV Dimers in Skin DNA of Patients with Basal Cell Carcinoma

Repair of UV Dimers in Skin DNA of Patients with Basal Cell Carcinoma

10.1158/1055-9965.epi-08-0248

Crossref journal-article

American Association for Cancer Research (AACR)

Cancer Epidemiology, Biomarkers & Prevention (1086)

Abstract

Abstract Epidemiologic studies suggest that exposure to sunlight is the primary etiologic agent for basal cell carcinoma. Formation of UV-induced DNA damage is believed to be a crucial event in the process leading to skin cancer. In this study, repair of photoproducts in DNA was followed in the skin of patients with basal cell carcinoma and control subjects. The subjects were exposed to 800 J/m2 Commission Internationale de 1'Éclairag of solar-simulating radiation on buttock skin. Biopsies were taken at 0 hour, 24 hours, and 3 weeks after the exposure. Two cyclobutane pyrimidine dimers, TT=C and TT=T, were measured using a sensitive 32P-postlabeling assay. Initial levels of both TT=C and TT=T differed between individuals in both groups. The levels of TT=T in patients with basal cell carcinoma and controls were similar (9.9 ± 4.0 and 9.2 ± 2.9 products per 106 normal nucleotides), whereas the level of TT=C was significantly lower in controls than in patients with basal cell carcinoma (6.2 ± 3.1 versus 10.9 ± 4.5 products per 106 normal nucleotides). The fractions of TT=T remaining after 24 hours and 3 weeks were significantly higher in patients with basal cell carcinoma (72% and 11%) compared with controls (48% and 5%). A slower removal in patients with basal cell carcinoma than in controls was indicated also for TT=C (52% versus 42% remaining at 24 hours); however, the difference between groups was not significant. When including data from our previously reported small-scale study, the fraction of dimers remaining at 24 hours was significantly higher in patients with basal cell carcinoma for both TT=C and TT=T. The data suggest that patients with basal cell carcinoma have a reduced capacity to repair UV-induced DNA lesions. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2388–92)

Authors 4

Dan Segerbäck (first)
Malgorzata Strozyk (additional)
Erna Snellman (additional)
Kari Hemminki (additional)

References 28 Referenced 10

Dates

Type	When
Created	16 years, 11 months ago (Sept. 3, 2008, 12:28 a.m.)
Deposited	3 years, 2 months ago (June 10, 2022, 3:57 a.m.)
Indexed	1 year, 11 months ago (Sept. 13, 2023, 3:26 p.m.)
Issued	16 years, 11 months ago (Sept. 1, 2008)
Published	16 years, 11 months ago (Sept. 1, 2008)
Published Online	16 years, 11 months ago (Sept. 2, 2008)
Published Print	16 years, 11 months ago (Sept. 1, 2008)

Funders 0

None

BibTeX

@article{Segerba_ck_2008, title={Repair of UV Dimers in Skin DNA of Patients with Basal Cell Carcinoma}, volume={17}, ISSN={1538-7755}, url={http://dx.doi.org/10.1158/1055-9965.epi-08-0248}, DOI={10.1158/1055-9965.epi-08-0248}, number={9}, journal={Cancer Epidemiology, Biomarkers & Prevention}, publisher={American Association for Cancer Research (AACR)}, author={Segerbäck, Dan and Strozyk, Malgorzata and Snellman, Erna and Hemminki, Kari}, year={2008}, month=sep, pages={2388–2392} }

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  "abstract": "<jats:title>Abstract</jats:title>\n               <jats:p>Epidemiologic studies suggest that exposure to sunlight is the primary etiologic agent for basal cell carcinoma. Formation of UV-induced DNA damage is believed to be a crucial event in the process leading to skin cancer. In this study, repair of photoproducts in DNA was followed in the skin of patients with basal cell carcinoma and control subjects. The subjects were exposed to 800 J/m2 Commission Internationale de 1'E\u0301clairag of solar-simulating radiation on buttock skin. Biopsies were taken at 0 hour, 24 hours, and 3 weeks after the exposure. Two cyclobutane pyrimidine dimers, TT=C and TT=T, were measured using a sensitive 32P-postlabeling assay. Initial levels of both TT=C and TT=T differed between individuals in both groups. The levels of TT=T in patients with basal cell carcinoma and controls were similar (9.9 \u00b1 4.0 and 9.2 \u00b1 2.9 products per 106 normal nucleotides), whereas the level of TT=C was significantly lower in controls than in patients with basal cell carcinoma (6.2 \u00b1 3.1 versus 10.9 \u00b1 4.5 products per 106 normal nucleotides). The fractions of TT=T remaining after 24 hours and 3 weeks were significantly higher in patients with basal cell carcinoma (72% and 11%) compared with controls (48% and 5%). A slower removal in patients with basal cell carcinoma than in controls was indicated also for TT=C (52% versus 42% remaining at 24 hours); however, the difference between groups was not significant. When including data from our previously reported small-scale study, the fraction of dimers remaining at 24 hours was significantly higher in patients with basal cell carcinoma for both TT=C and TT=T. The data suggest that patients with basal cell carcinoma have a reduced capacity to repair UV-induced DNA lesions. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2388\u201392)</jats:p>",
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