Polymorphisms of the CYP1A1 and GSTM1 gene involved in oral squamous cell carcinoma in association with a cigarette dose

被引:88
作者
Tanimoto, K
Hayashi, S
Yoshiga, K
Ichikawa, T
机构
[1] Hiroshima Univ, Sch Dent, Dept Oral & Maxillofacial Surg 1, Minami Ku, Hiroshima 7348553, Japan
[2] Saitama Canc Ctr, Dept Biochem, Inst Res, Ina, Saitama 3620806, Japan
来源
ORAL ONCOLOGY | 1999年 / 35卷 / 02期
关键词
CYP1A1; GSTM1; polymorphism; susceptibility; oral cancer;
D O I
10.1016/S1368-8375(98)00094-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The genetic polymorphisms of CYP1A1 and GSTM1 genes among 100 Japanese patients with oral squamous cell carcinomas (SCC) were investigated to evaluate the role of genetic susceptibility in carcinogenesis of the oral cavity. The presence of the rare homozygote of CYP1A1, m2/m2, was significantly more frequent in the patient group (15.0%) than the control group (8.0%) (Odds ratio (ORs) = 3.6 95% Confidential Interval (CI):1.4-9.5). The heterozygotic variant, m1/m2, was also frequently seen in oral SCC patients. This meant that the m2 allele was observed in more than half of the patients. The null genotype of GSTM1 was found in 43.0% of the patient group. This was not significantly different from the controls (40.0%). When the life time cigarette consumption dose of the patients was considered with respect to genotypes of CYP1A1, the mean smoking index (SI) of oral SCC patients with m2/m2 was found to be less than half of the mean SI among the patients with m1/m1 genotype (P < 0.02). The ORs of the m2/m2 genotype was found to be significantly high in a comparison of various subsites of the oral cavity, except for the floor of the mouth. Our results indicate that the rare homozygote of CYP1A1, m2/m2, is associated with increased risk of oral SCC, in particular, at low cigarette dose levels. The results also suggested that the involvement of such susceptibility in oral carcinogenesis might be different between the subsites of the oral cavity. (C) 1999 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:191 / 196
页数:6
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