Liu Fen, Pan Kaifeng, Zhang Xuemei, Zhang Yang, Zhang Lian, Ma Junling, Dong Caixuan, Shen Lin, Li Jiyou, Deng Dajun, Lin Dongxin, You Weicheng
Department of Cancer Epidemiology, Peking University School of Oncology, Beijing Institute for Cancer Research, Beijing Cancer Hospital, Beijing, China.
Gastroenterology. 2006 Jun;130(7):1975-84. doi: 10.1053/j.gastro.2006.03.021.
BACKGROUND & AIMS: To screen the genetic variants in cyclooxygenase-2 (COX-2), and evaluate their effects on COX-2 expression and risk of gastric cancer (GC) and its precursors, a population-based study was conducted in Linqu County, Shangdong Province, an area of China, a high-risk area of GC.
Genotypes were determined by polymerase chain reaction (PCR)-based denaturing high-performance liquid chromatography analysis in 248 GC cases and 1523 subjects with precancerous gastric lesions. COX-2 expression was detected by immunohistochemical analysis of biopsy specimens of 593 subjects selected at random from 1523 subjects. COX-2 transcriptional activity was examined by luciferase reporter gene assay.
We found an increased risk of GC in subjects with -1195 AA genotype (adjusted odds ratio [OR], 2.33; 95% confidence interval [CI]: 1.45-3.75). Stratified analysis indicated that an elevated risk of GC was observed in subjects carrying the AA genotype and Helicobacter pylori infection (OR, 3.88; 95% CI: 1.46-10.34) or smoking (OR, 7.02; 95% CI: 2.19-22.48), and a high expression of COX-2 was found in subjects with AA genotype (OR, 1.84; 95% CI: 1.09-3.10) compared with GG genotype. The prevalence of COX-2 expression positivity varied markedly by histologic status, and the OR (OR, 5.35; 95% CI: 2.64-10.8) was significantly increased for dysplasia compared with superficial gastritis/chronic atrophic gastritis. Furthermore, tissue homogenate with H pylori infection could significantly stimulate COX-2 promoter activity driven by -1195A compared with the -1195G containing counterparts.
These findings suggest that COX-2 polymorphisms may play an important role, at least in part, in developing GC in this high-risk population.
为筛查环氧化酶-2(COX-2)的基因变异,并评估其对COX-2表达以及胃癌(GC)及其癌前病变风险的影响,在中国山东省临朐县(一个GC高发地区)开展了一项基于人群的研究。
采用基于聚合酶链反应(PCR)的变性高效液相色谱分析法,对248例GC病例和1523例有胃癌前病变的受试者进行基因分型。从1523例受试者中随机选取593例受试者,通过免疫组织化学分析活检标本检测COX-2表达。采用荧光素酶报告基因检测法检测COX-2转录活性。
我们发现,-1195 AA基因型的受试者患GC的风险增加(校正比值比[OR],2.33;95%置信区间[CI]:1.45 - 3.75)。分层分析表明,携带AA基因型且感染幽门螺杆菌的受试者(OR,3.88;95% CI:1.46 - 10.34)或吸烟的受试者(OR,7.02;95% CI:2.19 - 22.48)患GC的风险升高,与GG基因型相比,AA基因型的受试者COX-2表达较高(OR,1.84;95% CI:1.09 - 3.10)。COX-2表达阳性的患病率因组织学状态而异,与浅表性胃炎/慢性萎缩性胃炎相比,发育异常的OR(OR,5.35;95% CI:2.64 - 10.8)显著升高。此外,与含-1195G的对应物相比,感染幽门螺杆菌的组织匀浆可显著刺激由-1195A驱动的COX-2启动子活性。
这些发现表明,COX-2基因多态性可能至少在一定程度上在这个高危人群的GC发生中起重要作用。