Lima Valeska Portela, de Lima Marcos Antonio Pereira, André Angela Rosa, Ferreira Márcia Valéria Pitombeira, Barros Marcos Aurélio Pessoa, Rabenhorst Sílvia Helena Barem
Department of Pathology and Forensic Medicine, Federal University of Ceará State, Porangabussu campus, Fortaleza, Ceará State, 60183-630, Brazil.
World J Gastroenterol. 2008 Feb 14;14(6):884-91. doi: 10.3748/wjg.14.884.
To investigate the interrelationship between H pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression.
seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation.
The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P = 0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori. However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups.
The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.
研究幽门螺杆菌（H pylori）与爱泼斯坦-巴尔病毒（EBV）感染在胃癌发生中的相互关系，重点关注p53突变以及c-Myc、Bcl-2和Bax的表达。
采用聚合酶链反应（PCR）检测71例胃癌组织中的幽门螺杆菌，原位杂交检测EBV。通过免疫组织化学检测c-Myc、Bcl-2和Bax的表达，采用单链构象多态性（SSCP）检测p53突变。
幽门螺杆菌和EBV的阳性率分别为94.4%和8.45%。大多数病例仅存在幽门螺杆菌感染。所有EBV阳性病例也均为幽门螺杆菌阳性。5.55%的病例未观察到任何感染因子。肠型肿瘤在合并感染组和未感染组中更为常见。未感染组中女性占主导，具有统计学意义（70.4%对29.6%，P = 0.039）。Bcl-2仅在单纯幽门螺杆菌感染组中检测到。然而，c-Myc和Bax在三组中均有检测到，但在合并感染组中的频率较低。p53突变在所有组中均存在，在幽门螺杆菌阳性组中频率最高。
胃癌中幽门螺杆菌感染率较高。所呈现的数据表明，根据两种被研究感染因子的存在情况，胃癌发生具有不同途径，提示幽门螺杆菌可能参与凋亡过程。EBV阳性组中c-Myc和Bax的低表达表明EBV可能抑制这些蛋白的表达。尽管如此，p53突变显示是一种相关改变，与两种感染因子均无关。
