摘要
Objective: 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 (8 nucleotides) (p <0.001). Conclusions: We suggest that genetic background and carcinogen exposure may increase the risk of developing oral cancer.
原文 | 英語 |
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頁(從 - 到) | 102-109 |
頁數 | 8 |
期刊 | Archives of Oral Biology |
卷 | 58 |
發行號 | 1 |
DOIs | |
出版狀態 | 已發佈 - 1月 2013 |
ASJC Scopus subject areas
- 耳鼻咽喉科
- 細胞生物學
- 牙科 (全部)