Shiotani Akiko, Iishi Hiroyasu, Ishiguro Shingo, Tatsuta Masaharu, Nakae Yukinori, Merchant Juanita L
Health Administration Center, Wakayama University, 930 Sakaedani, Wakayama 640-8510, Japan.
J Gastroenterol. 2005 Apr;40(4):337-44. doi: 10.1007/s00535-004-1549-9.
Gastric cancer is typically an end result of Helicobacter pylori-associated chronic gastritis. The pathogenesis is thought to involve effects on gastric mucosal epithelial cell turnover. In this study, we aimed to compare apoptosis and proliferation in the noncancer-containing mucosa of H. pylori-positive patients with early gastric cancer with these phenomena in H. pylori-positive controls.
Two specimens each were obtained from the greater and lesser curvatures of the corpus and from the greater curvature of the antrum. The histopathological grading used was the updated Sydney System. Apoptotic epithelial cells were detected using the terminal deoxy nucleotidyl transferase-mediated deoxy-uridine triphosphate (dUTP) biotin nick-end labeling (TUNEL) method. The expression of Ki 67 was evaluated by immunostaining.
Forty-five H. pylori-positive patients with endoscopic mucosal resection for early gastric cancer and 52 H. pylori-positive controls were studied. Gastric cancer was associated with a higher frequency of incomplete intestinal metaplasia (IM; odds ratio [OR], 19.1; 95% confidence interval [CI], 6.9-53.2; P < 0.001). The apoptotic index (AI) in the greater curvature of the corpus and the proliferation index (PI) in each part were significantly higher in cancer patients than in the control group. The median PI in the antrum was significantly higher in the incomplete IM group than that in the complete IM group (17.6 vs 12.6; P = 0.009). The PI and the AI in the greater curvature of the corpus correlated with the activity score, and the PI correlated with the IM score.
In the cancer patients, H. pylori-induced gastritis was associated with increased cell proliferation and apoptosis compared with mucosal findings in the controls. IM seems to be one of the most important factors affecting cell proliferation and may be one of the components of carcinogenesis that results in proliferation-dominant cell kinetics.
胃癌通常是幽门螺杆菌相关慢性胃炎的最终结果。其发病机制被认为涉及对胃黏膜上皮细胞更新的影响。在本研究中，我们旨在比较早期胃癌幽门螺杆菌阳性患者的非癌黏膜中的细胞凋亡和增殖情况与幽门螺杆菌阳性对照组中的这些现象。
从胃体大弯和小弯以及胃窦大弯各获取两份标本。采用的组织病理学分级是更新后的悉尼系统。使用末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸（dUTP）生物素缺口末端标记（TUNEL）法检测凋亡上皮细胞。通过免疫染色评估Ki 67的表达。
研究了45例接受内镜下黏膜切除术治疗早期胃癌的幽门螺杆菌阳性患者和52例幽门螺杆菌阳性对照。胃癌与不完全肠化生（IM）的较高发生率相关（优势比[OR]，19.1；95%置信区间[CI]，6.9 - 53.2；P < 0.001）。癌症患者胃体大弯处的凋亡指数（AI）和各部位的增殖指数（PI）均显著高于对照组。不完全IM组胃窦部的中位PI显著高于完全IM组（17.6对12.6；P = 0.009）。胃体大弯处的PI和AI与活动评分相关，PI与IM评分相关。
与对照组的黏膜表现相比，癌症患者中幽门螺杆菌诱导的胃炎与细胞增殖和凋亡增加相关。IM似乎是影响细胞增殖的最重要因素之一，可能是导致以增殖为主的细胞动力学的致癌过程的组成部分之一。
