Yang Gui-bin, Hu Fu-lian, Lü You-yong
Department of Gastroenterology, First Hospital, Peking University, Beijing 100034, China.
Zhonghua Yi Xue Za Zhi. 2003 Aug 10;83(15):1331-5.
To explore the relation between H. pylori infection and the development of gastric mucosa lesions, and to evaluate the effect of H. pylori infection on cell proliferation, p53 mutation, and MG-7 antigen expression in patients with gastric precancerous lesions.
One hundred and nine gastric biopsy specimens were divided into five groups of different gastric mucosa lesions according to pathologic findings and the results of mucosa histochemical staining: type I intestinal metaplasia (IM), type IIIM, type III IM, dysplasia (Dys) and gastric cancer (GC). H. pylori and its cagA status were assessed by microdissection/PCR method. Expression of P53 protein and MG-7 antigen were examined by immunohistochemical staining. AgNOR staining was performed for each specimen.
(1) Expression of P53 increased in more severe gastric mucosa lesion groups. The P53 expression rate in GC group was significantly higher than other groups (P < 0.05). There was no difference in expression of P53 between groups of different H. pylori status as while as different cagA status. (2) The expression of MG-7 in GC group was significantly higher than that in other groups (P < 0.05). There were no difference of expression of MG-7 between subgroups of different H. pylori infection status or cagA status in all groups (P > 0.05). (3) The counts of argyrophil protein of the nucleolar organizer regions (AgNORs) were significantly increased in more severe gastric mucosa lesion groups (P < 0.05), and were significantly higher in H. pylori positive and cagA positive specimens than in other specimens (P < 0.05).
Infection with H. pylori, particularly cagA-positive strains, is associated with the development of more severe gastric mucosa lesions; it seems to have effects on cell proliferation in patients with gastric precancerous lesions. Expression of P53 and MG-7 are earlier events in gastric cancer carcinogenesis.
探讨幽门螺杆菌（H. pylori）感染与胃黏膜病变发生发展的关系，评估H. pylori感染对胃癌前病变患者细胞增殖、p53突变及MG-7抗原表达的影响。
109份胃活检标本根据病理结果及黏膜组织化学染色结果分为5组不同胃黏膜病变：I型肠化生（IM）、II型IM、III型IM、异型增生（Dys）和胃癌（GC）。采用显微切割/聚合酶链反应（PCR）法检测H. pylori及其cagA状态。采用免疫组织化学染色检测P53蛋白和MG-7抗原表达。对每个标本进行核仁组成区嗜银蛋白（AgNOR）染色。
（1）P53表达在更严重的胃黏膜病变组中增加。GC组P53表达率显著高于其他组（P < 0.05）。不同H. pylori状态组及不同cagA状态组之间P53表达无差异。（2）GC组MG-7表达显著高于其他组（P < 0.05）。所有组中不同H. pylori感染状态或cagA状态亚组之间MG-7表达无差异（P > 0.05）。（3）核仁组成区嗜银蛋白（AgNORs）计数在更严重的胃黏膜病变组中显著增加（P < 0.05），H. pylori阳性和cagA阳性标本中的计数显著高于其他标本（P < 0.05）。
H. pylori感染，尤其是cagA阳性菌株感染，与更严重的胃黏膜病变发生有关；似乎对胃癌前病变患者的细胞增殖有影响。P53和MG-7表达是胃癌发生过程中的早期事件。
