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背景与目的:幽门螺杆菌(Helicobacterpylori,Hp)是确定的胃癌致癌因子,但其致癌的确切机制仍不清楚。p53、p21WAF1、p16为主要的细胞周期负调控基因。本研究旨在探讨胃癌及其有关病变中,上述3种抑癌基因的作用及其与幽门螺杆菌感染的关系。方法:应用HID-AB(pH2.5)-PAS、SP免疫组化染色及Warthin-Starry染色,对65例慢性萎缩性胃炎(chronicatrophicgastritis,CAG),93例肠上皮化生(intestinalmetaplasia,IM),94例胃上皮不典型增生(gastricepithelialdysplasia,GED)及60例胃癌(gastriccarcinoma,GC)中3种抑癌基因表达和幽门螺杆菌感染情况进行检测。结果:在胃癌发生的不同阶段,p53阳性表达率随病变发展而升高,在CAG、IMⅠ～Ⅱ、IMⅢ、GEDⅠ级、GEDⅡ～Ⅲ级及GC中分别为0、1.64%、6.25%、5.45%、23.08%、70.00%。p21WAF1和p16阳性表达率随病变发展而降低,p21WAF1阳性表达率分别为100%、95.08%、100%、100%、71.79%、45.00%,p16阳性表达率分别为83.08%、81.97%、78.13%、89.09%、69.23%、40.00%。三者表达在GEDⅡ～Ⅲ与GEDⅠ组间、GC与GEDⅡ～Ⅲ组间的差异均具有显著性(P<0.05)。同一病变中,Hp感染阳性组p53、p21WAF1及p16阳性表达率虽然高于Hp阴性组,但差异无显著性(P>0.05)。结论:p53突变及p21WAF1、p16失活
BACKGROUND & OBJECTIVE: Helicobacter pylori (Hp) is a definite oncogenic factor of gastric cancer, but its exact mechanism of carcinogenesis remains unclear. p53, p21WAF1, p16 as the main cell cycle negative regulation gene. This study aimed to investigate the role of the three tumor suppressor genes and their relationship with Helicobacter pylori infection in gastric cancer and its related diseases. Methods: 65 cases of chronic atrophic gastritis (CAG), 93 cases of intestinal metaplasia (IM), chronic myelogenous gastroenteritis (CAG) 94 cases of gastric epithelial dysplasia (GED) and 60 cases of gastric carcinoma (GC) in the three tumor suppressor gene expression and detection of Helicobacter pylori infection. Results: The positive rates of p53 in different stages of gastric cancer increased with the development of lesions. The positive rates of p53 were 0,1.64%, 6.25% and 5.45 in CAG, IMⅠ ~ Ⅱ, IMⅢ, GEDⅠ, GEDⅡ ~ Ⅲ and GC %, 23.08%, 70.00%. The positive expression rate of p21WAF1 and p16 decreased with the development of the lesion. The positive rate of p21WAF1 expression was 100.08%, 95.08%, 100%, 100%, 71.79% and 45.00%, respectively. The positive rates of p16 were 83.08%, 81.97% and 78.13% , 89.09%, 69.23%, 40.00%. The three expressions were between GEDⅡ-Ⅲ and GEDⅠgroup, and there was significant difference between GC and GEDⅡ-Ⅲgroup (P <0.05). In the same lesion, the positive rate of p53, p21WAF1 and p16 in Hp positive group was higher than that in Hp negative group, but the difference was not significant (P> 0.05). Conclusion: p53 mutation and p21WAF1, p16 inactivation