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

RESULTS

Oral Squamous Cell Carcinoma and Lifestyle. General demographic and clinical information for participants in both groups are provided in Table 1. There was no statistically significant difference in gender or age between case and control groups (p >0.05). However, smoking and drinking were significantly more common in individuals with OSCC than in controls (p <0.01). Genotype Distribution. For each of the enzyme encoding genes we investigated, the distribution of genotypes, significantly differed between cases and controls (all p <0.01). CYP1A1-MspI (m2/m2), EC-SOD (C/G), GSTT1 [–], GSTM1 [–] and ALDH2 (non G/G) genotypes were significantly more common in individuals with OSCC than in control individuals (p <0.01) (Table 2). Multiple Genotype Variants Distribution. Because there was a significant shift of the genotype frequencies observed in individuals with OSCC compared to controls, we also examined whether OSCC patients were more likely to carry multiple variant genotypes than healthy subjects. The combined distribution of CYP1A1-MspI (m2/ m2), ECSOD (C/G), GSTT1 [–], GSTM1 [–] and ALHD2 (non G/G) genotypes in both groups are provided in Table 3. Within the patient group, the majority of individuals (90.4%) had at least two of the variants. Namely, 1.9% of individuals were positive for five of the variant genotypes, 20.8% for four genotypes, 37.1% for three genotypes, 30.7% for two genotypes, 8.5% for only one variant genotype, and only 1.1% did not have any of the variant genotypes. In contrast, in the control group, the majority of individuals had one or no variants (51.6%). Thus, the presence of two or more variants in the OSCC population was significantly more common than in controls (p <0.01). Smoking Status and Gene Polymorphisms. Table 4 depicts the results of the analysis of CYP1A1-MspI (m2/ m2), EC-SOD (C/G), GSTT1 [–], GSTM1 [–] and ALHD2 (non G/G) variant genotype presence and smoking status. In individuals with OSCC, multiple variants and smoking were significantly more common compared to the control group; smoking in combination with multiple variant genotypes had a synergistic effect on cancer likelihood. Smokers with five variant genotypes were 32-times more likely to have OSCC. Furthermore, within the sub-population of smokers, SI was synergistic with multiple variant genotypes (Table 5). In the patient group, the presence of multiple variant genotypes and an SI >400 was significantly more common compared to the control group (p <0.01). Drinking Status and Gene Polymorphisms. A similar analysis was applied to CYP1A1-MspI (m2/m2), EC-SOD (C/G), GSTT1 [–], GSTM1 [–] and ALHD2 (non G/G) variant genotypes and alcohol consumption (Table 6). The presence of multiple variants and alcohol consumption was significantly more common in patients compared to the control group; furthermore, as with smoking, the drinking behavior and combined variant genotypes had a synergistic effect on the likelihood of cancer. The synergistic effect of the DI and combined expression of variant genotypes is depicted in Table 7. In the patient group, the presence of multiple variants and a DI >3000 was significantly more common compared to the control group (p <0.01). Analysis of Combined Smoking/Drinking Status and Gene Polymorphisms. Table 8 displays the results of the analysis of the presence of variant genotypes combined with smoking and drinking status. In the patient group, there were significantly more patients who had multiple variants and were positive for both smoking and drinking history as compared to the control group.



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