| Summary: | 碩士 === 長庚大學 === 基礎醫學研究所 === 88 === Abstract
Oral cancer is one of the ten leading causes of cancer death in Taiwan. According to Health and Vital Statistics Republic of Chine in 1998,oral cancer is the seventh leading causes of cancer death and the fifth for man. The mortality rate of oral cancer was 9.6 per 100,000 in 1998 and gradually increasing year by year. Epidemiological studies have indicated that cigarette smoking, alcohol drinking and betel quid chewing are associated with the development of oral cancer.
One hundred and eighty-seven oral squamous cell carcinomas(OSCC) were investigated for the association between cigarette smoking, alcohol drinking and betel quid chewing, genotypes of GSTT1 and GSTM1 genes, the presence of EBV DNA and p53 gene mutations. Genotypes of GSTT1 and GSTM1 genes, the presence of EBV DNA and p53 gene mutations were analyzed by polymerase chain reaction, single strand conformation polymorphism and DNA sequencing. The history of cigarette smoking, alcohol drinking and betel quid chewing was obtained by questionnaire.
The following results were obtained (1)The most common sites for the OSCCs are tongue and bucca. This is similar to the report from prevalent tobacco chewing countries. (2)Among this 187 OSCC patients , 81.8%, 52.8% and 74.4% had the history of cigarette smoking, alcohol drinking and betel quid chewing, respectively. (3)The patients with malignant neoplasm at oropharynx and hypopharynx have a higher rate of alcohol drinking than those at other sites. (4)Ninety-one of the 187 OSCCs (48.7%) showed p53 gene mutations at exon 5-9. The most common mutated region were at exon 5(33%) and exon 8(31%). (5)Alcohol drinking was associated with a higher rate of p53 gene mutation in patients with betel quid chewing(OR=2.47;p=0.02).(6)The major types of p53 gene mutation were GC→AT(40.8%), GC→TA(17.1%), GC→CG(10.5%) and deletion(14.5%).When compared to the findings from other countries with tobacco chewing, Taiwan OSCCs showed higher rates of deletion and GC→CG changes with a lower rates AT→GC changes. The hot-spots of p53 gene mutation were found in order at codon 273, 152, 175, 245 and 248. (7)Within GSTT1 non-null OSCC patients, subjects with GSTM1 null genotype showed to have a higher rates of p53 gene mutation than those with non-null genotype(OR=2.29;p=0.11).However, the genotype of GSTM1 and GSTT1 did not associate with p53 gene mutation by it self. (8)Due to a low EB virus infection rate (6%), the relationship between EB virus and OSCC, could not be analyzed further .
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