SUSCEPTIBILITY TO ORAL SQUAMOUS CELL CARCINOMA: CORRELATION WITH VARIANTS OF CYP1A1-MspI, GSTT1, GSTM1, ALDH2, EC-SOD AND LIFESTYLE FACTORS
Dong T-T, Wang L-J, Liu L-Z, Ma S-N
*Corresponding Author: Mrs. Ting-Ting Dong, General Hospital of Daqing Oil Field, No. 9 Zhongkang Street, Saertu District, Daqing 163001, Heilongjiang Province, People’s Republic of China. Tel: +86-459-599-4114. Fax: +86-459-580-5247. Email: tingtingdong_139@163.com
page: 61

DISCUSSION

The pathogenesis of OSCC is complex, involving combined action of a variety of environmental and genetic factors [11-13]. Smoking and drinking are the main risk factors for OSCC [14,15]. Our findings confirm that smoking and drinking were significantly more frequent in individuals with OSCC than in the control individuals. Heavy cigarette and alcohol consumption were also significantly higher in the OSCC group compared to the control group. The CYP1A1 is a member of the cytochrome P450 family involved in the metabolism of exogenous materials, encoding aryl hydrocarbon hydrolase (AHH), and activating polycyclic aromatic hydrocarbon and aromatic amine [16]. Our results showed that the distribution of genotypes for CYP1A1-MspI was significantly different between the patient group and the control group, and that the CYP1A1- MspI (m2/m2) genotype may increase susceptibility to OSCC. This finding, aligned with prior studies, shed light on the involvement of the CYP1A1-MspI polymorphism in carcinogenesis through modified enzymatic activity [16]. Our results also confirmed the results of a meta-analysis which found that CYP1A1-MspI increased the odds of OSCC, specifically among Asian populations [30]. Superoxide dismutase is generally considered as the first line antioxidative defense in the body [17]. This enzyme can be highly effective against ROS to protect the cells and tissues from oxidative stress [18]. The SOD dysregulation is correlated with growth of human malignant tumors [19,20]. Further, EC-SOD appears to be important for tumor formation [21-23], and is correlated with OSCC [24]. Our study mirrored the earlier studies that indicated EC-SOD association with OSCC and showed a significant difference in distribution of EC-SOD genotypes between the patient and control groups [24]. The GST polymorphisms are also correlated with cancer susceptibility. Glutathione S-transferase can catalyze the binding of electrophilic carcinogens and glutathione, to metabolize compounds that are easily soluble in water and excrete them. GSTM1/GSTT1 has been previously associated with susceptibility to oral carcinomas [25,31]. Our study confirmed that GSTM1[–]/GSTT1[–] genotypes are correlated with susceptibility to OSCC. Animal studies have found that the in vivo metabolite of ethanol, acetaldehyde, has significant carcinogenic effects [26,27], and ALDH2 is the main enzyme to metabolize acetaldehyde in the liver. Furthermore, ALDH2 gene polymorphism is correlated with a variety of tumors [28-30,32]. Our study confirmed the correlation between ALDH2 (non G/G) genotypes and increased susceptibility to OSCC. Interestingly, our study also found significant differences in the prevalence of combined CYP1A1-MspI (m2/ m2), EC-SOD (C/G), GSTT1 [–], GSTM1 [–] and ALHD2 (non G/G) variant genotypes between the patient and control groups. In the patient group, the percentage of patients with a combination of variant genotypes (more than two genotypes) was significantly higher than that of the control group; the relative risks of OSCC in such patients were significantly increased. Previous studies have shown that OSCC patients are more likely to carry multiple variants and have a history of smoking or drinking; the interaction of two or more of these factors enhances risk [3,5,29, 30,32]. Our simultaneous analyses confirmed these previous results, as individuals with both multiple variant genotypes and a smoking and drinking history exhibited a significantly higher risk of OSCC. Therefore, OSCC risk increases with the increasing amount and period of smoking and drinking. Further investigations and studies of the effects of these gene and environmental interactions is paramount to an earlier diagnosis of OSCC. More studies of non Asian populations is another avenue of research worth undertaking.



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