CHUN-YI CHUANGCHUNG-HAN HSIN2026-10-162026-10-162013-01-01Pure ID: 15096011Pure UUID: 65eb8218-dbea-4ccc-8991-3b9a865fa62310.1016/j.archoralbio.2012.06.004https://www.scopus.com/pages/publications/84870455862https://scholars.csmu.edu.tw/handle/123456789/27327Objective: Most reports have shown that PAH-related DNA adducts are positively correlated with the smoking status of oral cancer patients. However, these reports did not focus on a specific carcinogen in cigarette smoke. The purpose of this study was to elucidate the role of the BPDE (7,8-dihydroxy-anti- 9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene)-DNA adduct in the development of oral cancer in Taiwanese patients. Design: We enrolled 158 oral cancer patients and 64 non-cancer controls to investigate whether there were differences in susceptibility to cigarette smoke exposure in the formation of DNA adducts between cancer patients and controls. Immunohistochemistry and ELISA (enzyme-linked immunosorbent assay) were used to evaluate BPDE-DNA adduct levels in this study. Results: Our data showed that the BPDE-DNA adduct levels were positively correlated with gender, smoking status, betel nut chewing and alcohol consumption. The difference in DNA adduct levels could be explained by genetic polymorphisms of glutathione S-transferase M1 (GSTM1), but not by cytochrome P-4501A1 (CYP1A1). Patients with high DNA adduct levels (≧34.03 adducts/108 nucleotides) had an approximately 9.936-fold risk of oral cancer compared with those with low DNA adduct levels (<34.03 adducts/108 nucleotides) (p < 0.001). Conclusions: We suggest that genetic background and carcinogen exposure may increase the risk of developing oral cancer.8enjournal article