Repair of UV dimers in skin DNA of patients with basal cell carcinoma.

2.50
Hdl Handle:
http://hdl.handle.net/10146/83596
Title:
Repair of UV dimers in skin DNA of patients with basal cell carcinoma.
Authors:
Segerback, Dan; Strozyk, Malgorzata; Snellman, Erna; Hemminki, Kari
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/m(2) Commission Internationale de 1'Eclairag 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 (32)P-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 10(6) 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 10(6) 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.
Citation:
Cancer Epidemiol. Biomarkers Prev. 2008, 17 (9):2388-2392
Journal:
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
Issue Date:
Sep-2008
URI:
http://hdl.handle.net/10146/83596
DOI:
10.1158/1055-9965.EPI-08-0248
PubMed ID:
18768508
Additional Links:
http://cebp.aacrjournals.org/content/17/9/2388.long
Type:
Article
Language:
en
ISSN:
1055-9965
Sponsors:
Dan Segerbäck is a partner in the European Union–sponsored Network of Excellence Environmental Cancer and Individual Susceptibility.
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorSegerback, Danen
dc.contributor.authorStrozyk, Malgorzataen
dc.contributor.authorSnellman, Ernaen
dc.contributor.authorHemminki, Karien
dc.date.accessioned2009-10-06T11:00:39Z-
dc.date.available2009-10-06T11:00:39Z-
dc.date.issued2008-09-
dc.identifier.citationCancer Epidemiol. Biomarkers Prev. 2008, 17 (9):2388-2392en
dc.identifier.issn1055-9965-
dc.identifier.pmid18768508-
dc.identifier.doi10.1158/1055-9965.EPI-08-0248-
dc.identifier.urihttp://hdl.handle.net/10146/83596-
dc.description.abstractEpidemiologic 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/m(2) Commission Internationale de 1'Eclairag 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 (32)P-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 10(6) 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 10(6) 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.en
dc.description.sponsorshipDan Segerbäck is a partner in the European Union–sponsored Network of Excellence Environmental Cancer and Individual Susceptibility.en
dc.language.isoenen
dc.relation.urlhttp://cebp.aacrjournals.org/content/17/9/2388.longen
dc.subjectUV lighten
dc.subjectBasal cell carcinomaen
dc.subjectDNA repairen
dc.subjectPyrimidine dimersen
dc.subjectPostlabelingen
dc.subject.meshAdult-
dc.subject.meshAged-
dc.subject.meshAged, 80 and over-
dc.subject.meshButtocks-
dc.subject.meshCarcinoma, Basal Cell-
dc.subject.meshCase-Control Studies-
dc.subject.meshChromatography, High Pressure Liquid-
dc.subject.meshDNA Damage-
dc.subject.meshDNA Repair-
dc.subject.meshDNA, Neoplasm-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshPyrimidine Dimers-
dc.subject.meshRisk-
dc.subject.meshSkin-
dc.subject.meshSkin Neoplasms-
dc.subject.meshSunlight-
dc.titleRepair of UV dimers in skin DNA of patients with basal cell carcinoma.en
dc.typeArticleen
dc.identifier.journalCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncologyen

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