Study On The Relationship Between Smoking And Oral Tumor

Objective: To study the relationship between smoking and the development of Warthin's tumor of the parotid gland. To study the genetic toxic effect of cigarette smoking on human exfoliated oral mucosa cells. To study the expression of P53 and P16 protein and to probe the relationship between expression of suppressor gene p53 and P16 and smoking.In order to explore the biomarker of smoker.Methods: The smoking history was surveyed in 60 cases with Warthin's tumor of parotid gland and 140 cases with pleomorphic adenoma in parotid gland served as the controls. In order to exclude sex and age as possible confounders, in males only and in patients over 40 years of age, the result was reevaluated. The DNA damage of exfoliated oral mucosa cells was detected with single cell gel electrophoresis (SCGE) in 24 smokers and 17 non-smokers, while some dangerous factors such as age and gender are also recorded. The tail length and frequency of comet cells were used to measure DNA damage. The expressions of p53 and p16 gene protein were detected in 32 cases of smokers and in 22 cases of nonsmokers with the immunohistochemical technique (SP method). SPSS and SAS software were used for analysis.Results: The percentage of smoker in patients with Warthin's tumor (73.33%) was much higher than that of patients with pleomorphic adenoma in parotid gland (15.71%). Morever, the amount of smoking was greater and the smoking history was longer in patients with Warthin's tumor. When the male and the patients over 40 year of age were analysed respectively, the same results were showen. Smokers had a larger tail length and frequency of comet cells than that of the nonsmokers, the tail lengths were(2.35 ± 0.08 μ m) and(0.92±0.06μ m) respectively, the frequency of comet cells were ( 18.16%) and (4.39%) respectively, the difference was significant(P<0.001) After adjusting for age and gender ,the smokers had a significant effect in the tail length and frequency of comet cells . The positive expression rates of p53 gene in smokers(90.91%) was higher than innonsmokers(46.88%), there was a significant difference(P<0.05).When the amounts and the years of smoking increased, the expression rate of p53 gene protein increased. The positive expression rates of pi 6 gene protein was no difference in smokers (54.55%) and nonsmokers (68.74%), but it is higher in cases of oral cancer than that of benign tumor and normal tissue, and there was ten(10/14) cases of low differentiating oral squamous carcinoma in the abnormal expression of pi 6 gene.Conclusion: This case-control study suggests that smoking is an etiologic factor in the development of Warthin's tumor of the parotid gland. Smoking can induce DNA damage of the exfoliated oral mucosa cells ,and a dose-response relationship was observed.Tobacco has an important effects on carcinogenesis.The consumption of tobacco > the period of smoking (year) and oral lesions had relationship with the tail length and frequency of comet cells. SCGE can reflect the DNA damage caused by chemical poison and could be used in molecular study. Smoking may stimulate the mutation of p53 gene, perhaps it may play an important role in the carcinogenesis of oral mucous. No significant relationship was found among the expression of the pl6 gene and smoking. But the pi6 abnormal expression is correlated closely with the oral cancer. This study showed that cigarette smoking is one of the important mutagenic factors that caused damage to human genetic materials.