幽门螺杆菌感染胃黏膜病变基因表达和细胞生物学行为

目的　研究幽门螺杆菌(Helicobacterpylori，Hp)感染胃黏膜病变的多基因表达和细胞生物学行为。方法　327例患者经胃镜及手术的胃黏膜病变标本，应用免疫组化染色法，检测p53、p16、bcl-2和环氧合酶同工酶-2(COX-2)蛋白的表达。Hp感染由快速尿素酶试验结合组织学检查/

Multiple genetic alterations and cellular biological behavior in gastric mucosal lesions with Helicobacter pylori infection

Objective To investigate the expression of multiple genes and the behavior of cellular biology in gastric mucosal lesions with Helicobacter pylori (H. pylori ) infection. Methods Tissue samples from 327 patients underwent endoscopy and surgical resection were studied. ABC immunohistochemical staining was used to detect the expression of p53, p16, bcl-2, and cyclooxygenase-2 (COX-2) proteins. H. pylori was determined by rapid urease test combined with histological examination/14C urea breath test. Cellular image analysis was performed in 66 patients with intestinal metaplasia (IM) and/or dysplasia (DYS). Results The positive expression rate of p53 in gastric cancer was significantly higher than that in DYS (P＜0.05). p16 expression in chronic atrophic gastritis, IM or DYS with H. pylori positive was significantly lower than that with H. pylori negative ( P＜0.05, P＜0.01 ), bcl-2 or COX-2 expression of IM or DYS with H. pylori positive was significantly higher than that with H. pylori negative. (P＜0.05). The mean number of most parameters of cellular image analysis in H. pylori positive group was significantly higher than that in H. pylori negative group (P＜0.05 or P＜0.01). Conclusions p16, bcl-2, and COX-2 but not p53 gene may play a role in the early development/promotion of gastric cancer and are associated with H. pylori infection. p53 gene is relatively late event in stomach tumorigenesis. There is more cellular-biological behavior of malignant tumor in gastric precancerous lesions with H. pylori infection.