Repair capacity for UV light induced DNA damage associated with risk of nonmelanoma skin cancer and tumor progression.

Published

Journal Article

PURPOSE: To examine the role of suboptimal DNA repair capacity (DRC) for UV light-induced DNA damage in the development of nonmelanoma skin cancer (NMSC) and tumor progression. EXPERIMENTAL DESIGN: We conducted a hospital-based case-control study of 255 patients with newly diagnosed NMSC [146 with basal cell carcinoma (BCC) and 109 with squamous cell carcinoma (SCC)] and 333 cancer-free controls. We collected information on demographic variables and risk factors from questionnaires, tumor characteristics from medical records, and lymphocytic DRC phenotype by the host-cell reactivation assay. Multivariable logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI). RESULTS: Overall, there was a relative 16% reduction in DRC in NMSC patients compared with controls (P < 0.001 for BCC and for SCC, respectively). DRC below the controls' median value was associated with increased risk significantly for BCC (OR, 1.62; 95% CI, 1.07-2.45) but borderline for SCC (OR, 1.63; 95% CI, 0.95-2.79) after adjustment for age, sex, and other assay-related covariates. When the highest tertile of controls' DRC was used as the reference, the intermediate and low DRC were associated with a statistically significant trend for increasing risk for both BCC (P(trend) = 0.007) and SCC (P(trend) = 0.020). However, patients with aggressive or multiple SCC tended to have a higher DRC than those with nonaggressive or single SCC. CONCLUSIONS: Reduced DRC is an independent risk factor for BCC and single or nonaggressive SCC but not for multiple primaries, local aggressiveness, or recurrence of NMSC.

Full Text

Duke Authors

Cited Authors

  • Wang, L-E; Li, C; Strom, SS; Goldberg, LH; Brewster, A; Guo, Z; Qiao, Y; Clayman, GL; Lee, JJ; El-Naggar, AK; Prieto, VG; Duvic, M; Lippman, SM; Weber, RS; Kripke, ML; Wei, Q

Published Date

  • November 1, 2007

Published In

Volume / Issue

  • 13 / 21

Start / End Page

  • 6532 - 6539

PubMed ID

  • 17975167

Pubmed Central ID

  • 17975167

International Standard Serial Number (ISSN)

  • 1078-0432

Digital Object Identifier (DOI)

  • 10.1158/1078-0432.CCR-07-0969

Language

  • eng

Conference Location

  • United States