title: Repair capacity for UV light induced DNA damage associated with risk of nonmelanoma skin cancer and tumor progression.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: Department of Epidemiology,The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
authors.forename: Li-E
authors.initials: LE
authors.lastname: Wang
authors.forename: Chunying
authors.initials: C
authors.lastname: Li
authors.forename: Sara S
authors.initials: SS
authors.lastname: Strom
authors.forename: Leonard H
authors.initials: LH
authors.lastname: Goldberg
authors.forename: Abenaa
authors.initials: A
authors.lastname: Brewster
authors.forename: Zhaozheng
authors.initials: Z
authors.lastname: Guo
authors.forename: Yawei
authors.initials: Y
authors.lastname: Qiao
authors.forename: Gary L
authors.initials: GL
authors.lastname: Clayman
authors.forename: J Jack
authors.initials: JJ
authors.lastname: Lee
authors.forename: Adel K
authors.initials: AK
authors.lastname: El-Naggar
authors.forename: Victor G
authors.initials: VG
authors.lastname: Prieto
authors.forename: Madeleine
authors.initials: M
authors.lastname: Duvic
authors.forename: Scott M
authors.initials: SM
authors.lastname: Lippman
authors.forename: Randal S
authors.initials: RS
authors.lastname: Weber
authors.forename: Margaret L
authors.initials: ML
authors.lastname: Kripke
authors.forename: Qingyi
authors.initials: Q
authors.lastname: Wei
mesh_terms: D000328:Adult; D000368:Aged; D002280:Basal Cell Carcinoma / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000473:pathology; D016022:Case-Control Studies; D004249:DNA Damage; D004260:DNA Repair; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D012008:Recurrence; D012306:Risk; D012878:Skin Neoplasms / Q000209:etiology* / Q000473:pathology*; D014466:Ultraviolet Rays