© 2005 Oxford University Press
ARTICLE |
In Vitro Sensitivity to Ultraviolet B Light and Skin Cancer Risk: A Case–Control Analysis
Affiliations of authors: Departments of Epidemiology (L-EW, PX, SSS, CIA, MRS, QW), Surgical Oncology (JEL, MIR, PFM, JEG, JNC), Pathology (VGP), Dermatology (MD), Head and Neck Surgery (GLC, RSW), and Clinical Cancer Prevention (SML), The University of Texas M. D. Anderson Cancer Center, Houston, and DermSurgery Associates, Houston, TX (LHG)
Correspondence to: Qingyi Wei, MD, PhD, Department of Epidemiology, Unit 1365, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030 (e-mail: qwei{at}mdanderson.org).
Background: Mutagen sensitivity, measured as mutagen-induced chromatid breaks per cell in primary lymphocytes in vitro, has been used to study susceptibility to various epithelial cancers. Patients with xeroderma pigmentosum are highly sensitive to ultraviolet (UV) light due to inherited defects in DNA repair and have a 1000-fold higher risk of UV-induced skin cancer than the general population. However, an association between UV-induced chromosomal aberrations and risk of skin cancer in the general population has not been established. Methods: We assessed in vitro UVB-induced chromatid breaks in a hospital-based case–control study. The study included 469 patients with skin cancer (231 with nonmelanoma skin cancer [NMSC] and 238 with cutaneous malignant melanoma [CMM]) and 329 cancer-free control subjects. Multivariable logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). All statistical tests were two-sided. Results: Compared with the frequency of UVB-induced chromatid breaks per cell in control subjects (mean = 0.28 breaks per cell, 95% CI = 0.27 to 0.30), that in NMSC patients (basal cell carcinoma [BCC], n = 143, mean = 0.36 breaks per cell, 95% CI = 0.33 to 0.39 and squamous cell carcinoma [SCC], n = 88, mean = 0.35 breaks per cell, 95% CI = 0.32 to 0.38) was higher (P = .001 and P<.001, respectively), but that in CMM case patients (mean = 0.30 breaks per cell, 95% CI = 0.28 to 0.33) was not (P = .22). A frequency of chromatid breaks per cell above the median of control subjects was associated with nearly threefold increased risks for BCC (OR = 2.78, 95% CI = 1.79 to 4.30) and SCC (OR = 2.62, 95% CI = 1.50 to 4.60), but not with an increased risk of CMM. A dose–response relationship was evident between mutagen sensitivity and risk for both BCC (Ptrend<.001) and SCC (Ptrend<.001). Multiplicative interactions between mutagen sensitivity and sun exposure variables on risk, particularly for sunburn in BCC and hair color, tanning ability, and family history of skin cancer in SCC, were seen for NMSC but not CMM. Conclusions: UVB-induced mutagen sensitivity may play a role in susceptibility to NMSC but not to CMM.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  D. Segerback, M. Strozyk, E. Snellman, and K. Hemminki Repair of UV Dimers in Skin DNA of Patients with Basal Cell Carcinoma Cancer Epidemiol. Biomarkers Prev., September 1, 2008; 17(9): 2388 - 2392. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Leng, C. A. Stidley, A. M. Bernauer, M. A. Picchi, X. Sheng, M. A. Frasco, D. Van Den Berg, F. D. Gilliland, R. E. Crowell, and S. A. Belinsky Haplotypes of DNMT1 and DNMT3B are associated with mutagen sensitivity induced by benzo[a]pyrene diol epoxide among smokers Carcinogenesis, July 1, 2008; 29(7): 1380 - 1385. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L.-E Wang, P. Xiong, H. Zhao, M. R. Spitz, E. M. Sturgis, and Q. Wei Chromosome Instability and Risk of Squamous Cell Carcinomas of Head and Neck Cancer Res., June 1, 2008; 68(11): 4479 - 4485. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Qureshi, F. Laden, G. A. Colditz, and D. J. Hunter Geographic Variation and Risk of Skin Cancer in US Women: Differences Between Melanoma, Squamous Cell Carcinoma, and Basal Cell Carcinoma Arch Intern Med, March 10, 2008; 168(5): 501 - 507. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L.-E Wang, C. Li, S. S. Strom, L. H. Goldberg, A. Brewster, Z. Guo, Y. Qiao, G. L. Clayman, J. J. Lee, A. K. El-Naggar, et al. Repair Capacity for UV Light Induced DNA Damage Associated with Risk of Nonmelanoma Skin Cancer and Tumor Progression Clin. Cancer Res., November 1, 2007; 13(21): 6532 - 6539. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Lu, L.-E Wang, P. Xiong, E. M. Sturgis, M. R. Spitz, and Q. Wei 172G>T variant in the 5' untranslated region of DNA repair gene RAD51 reduces risk of squamous cell carcinoma of the head and neck and interacts with a P53 codon 72 variant Carcinogenesis, May 1, 2007; 28(5): 988 - 994. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Wu, J. Gu, and M. R. Spitz Mutagen Sensitivity: A Genetic Predisposition Factor for Cancer Cancer Res., April 15, 2007; 67(8): 3493 - 3495. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Erdei, S.-J. Lee, Q. Wei, L.-E. Wang, Y.-S. Song, D. Bovbjerg, and M. Berwick Reliability of mutagen sensitivity assay: an inter-laboratory comparison Mutagenesis, July 1, 2006; 21(4): 261 - 264. [Abstract] [Full Text] [PDF]
|
|