Abstract 1864: The association between XPC polymorphism and cooking fume exposure in the risk of female lung adenocarcinoma: a case-control study

• Published in: Cancer research (Chicago, Ill.) Ill.), 2010-04, Vol.70 (8_Supplement), p.1864-1864
• Main Authors: Yang, Shi-Yi, Li, Yao-Jen, Liao, Kuo-Meng, Chen, Chuen-Fei, Chen, Chien-Jen
• Format: Article
• Language: English
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM10-1864

Purpose: Lung cancer is the leading cause of cancer death in Taiwanese women who mainly have no smoking history throughout their lives. Thus, the identification of etiologic factors leading to lung adenocarcinoma among female nonsmokers is important. The XPC located on chromosome 3p25, involving in nucleotide excision repair system (NER) that repairs the DNA damages to maintain the genome integrity. We evaluated the association between XPC polymorphism, codon 939 Lys/Gln, Cooking fume exposure and the risk of female lung adenocarcinoma. Methods: The polymorphism was determined in 1030 cases with lung adenocarcinoma and 1087 healthy hospital controls and assayed by TaqMan assay, Unconditional multiple logistic regression was used to estimate odds ratio (OR) and 95% confidence intervals (CI). Results: Patients with Gln/Gln and Gln/Lys alleles had 1.3 and 1.7 fold (95% CI = 1.0-1.8 and 1.1-2.6, respectively) evaluated risk of developing lung adenocarcinoma compared with patients with Lys/Lys alleles after the adjustment for age, father's ethnicity, schooling years, family history of lung cancer, history of tuberculosis, cooking fume, BMI, arsenic-exposed area, active cigarette smoking, and exposure to environmental tobacco smoke. Besides, the interactions between the genetic polymorphism and environmental factors including cooking fume exposure and when to started cooking were also tested. Among those with cooking fume exposure, patients combined Gln/Gln and Gln/Lys genotype showed a 3.4 fold (95%CI, 1.1-10.2) risk of developing lung adenocarcinoma compared to those with Lys/Lys genotype, while among those without cooking fume exposure, combined Gln/Gln and Gln/Lys genotype had a slightly 1.2 fold (95%CI, 0.9-1.5) risk of developing lung adenocarcinoma compared to those with Lys/Lys genotype. In addition, gene dosage and environmental effect showed that patients combined Gln/Gln and Gln/Lys genotype in the group who exposed to cooking fume had a 6.1 fold (95%CI, 2.8-13.3) risk compared to those with Lys/Lys genotype among group without cooking fume exposure. Furthermore, exposed for cooking fume was categorized into non-cooking, and cooking with or without fume extractor, gene-environment interaction analysis showed that combined Gln/Gln and Gln/Lys genotype among cooking without fume extractor, had a 4.7 fold (95%CI, 2.8-13.3) risk compared to those with Lys/Lys genotype among group without cooking fume exposure. Conclusions: Our findings suggested that the