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Arch Oral Biol. 2013 Jan;58(1):102-9. doi: 10.1016/j.archoralbio.2012.06.004. Epub 2012 Jul 17.

BPDE-like DNA adduct level in oral tissue may act as a risk biomarker of oral cancer.

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1
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.

Abstract

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/10(8) nucleotides) had an approximately 9.936-fold risk of oral cancer compared with those with low DNA adduct levels (<34.03 adducts/10(8) nucleotides) (p<0.001).

CONCLUSIONS:

We suggest that genetic background and carcinogen exposure may increase the risk of developing oral cancer.

[Indexed for MEDLINE]

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