胃癌变过程中幽门螺杆菌感染与Ki67和P27蛋白表达的意义

目的探讨胃癌变过程中胃黏膜上皮细胞幽门螺杆菌（Hp）感染与细胞增生及抑癌基因P27蛋白表达的意义。方法用快速尿素酶法、美蓝法及免疫组化法联合检测312例胃镜活检标本Hp感染率，其中慢性浅表性胃炎（CSG）112例、慢性萎缩性胃炎（CAG）100例、胃癌（GC）100例。并采用免疫组化技术分别检测标本中Ki67和P27蛋白的表达，观察Hp感染对Ki-67和P27蛋白表达的影响。结果运用三种方法联合检测，所有病例、CSG、CAG和GC中Hp感染率分别为49．0％（158／312）、25．9％（29／112）、53．0％（53／100）、71．0％（71／100）。CAG组明显高于CSG组（P〈0．05）；GC组明显高于CAG组和CSG组P〈0．05，P〈0．01）。所有病例中均能检测到Ki=67和P27蛋白的表达，Ki67在CSG、CAG、GC中的阳性表达率为35．7％（40／112），58．0％（58／100），64．0％（64／100）。且GC组明显高于CSG组（P〈0．05）；P27在CSG、CAG、GC中的表达率为36．6％（41／112），32．0％（32／100），29．0％（29／100）。随着病变进展，P27的表达逐渐下降，但差异无统计学意义（P〉0．05）。结论Hp在癌组织阳性率明显高于非癌组织，胃癌可能是Hp长期感染与其他因素共同作用的结果。Hp感染可诱导胃黏膜Ki-67和P27的表达异常，使抑制上皮生长与调节细胞凋亡信号传导的转化因子受体数目减少，引起胃黏膜上皮细胞的过度增生，同时也与抑癌基因P27的失活有关。

Significance of helicobacter pylori infection and expression of Ki67 and P27 during carcinogenesis of gastric mucosa.

Objective To study the significance of helieobacter pylori （ H. pylori） infection and expression of Ki67 and P27 protein dur- ing carcinogenesis of gastric mucosa. Methods Rapid urea enzymatic, methylene blue method and immunohistochemical method were employed to detect of H. pylori in 312 cases of gastroscope biopsy specimens. These specimens included 112 cases of chronic superficial gastritis （ CSG）, 100 cases of chronic atrophic gastritis （CAG） and 100 cases of gastric cancer （GC）. Immunohistochemical technique also was used to determine the expression of K - i67 and 1727 protein in respectively test specimens. The aim of this expression is to explore relationship between the H. pylori and the expression of K - i67 and P27 protein. Results The rates of H. pylori infection detected by three methods in total cases, CSG, CAG and GC were 49.0% （158/312） , 25.9% （29/112） , 53.0% （53/100） and 71.0% （71/100） , respectively. The rates of the CAG group were more increased significantly than the CSG group （ P 〈 0.05 ）. and the rates of GC group were increased significantly than the CAG group and CSG group （ P 〈 0.05, P 〈 0.01 ）. Expression of K - i67 and 1：r27 protein were detected in all cases. The positive rates of K - i67 in CSG, CAG, and GC respectively were 35.7% （40/112）, 58.0% （58/100）, 64.0% （64/100）. The rates of the CAG group were more increased significantly than the CSG group （ P 〈0.05）. The positive rates of P27 protein in CSG, CAG, and GC respectively were 36.6% （41/112）, 32.0% （32/ 100）, 29.0% （29/100）. With the progress of carcinogenesis, the expression of P27 protein is decreasing, but there were no statistical signifi- cance between groups （ P 〉 0.05 ）. Conclusion The rates of H. pylori infection are higher significantly in cancerous lesion than those of non - cancerous lesion. Cancer of the stomach may be outcome of long - term H. pylori infection combined other factors. The rates of H. pylori infection are higher, the more serious are lesion of the gastric mucosal. H. pylori infection can induce abnormal expression of K - i67 and P27 protein of gastric mucosa, inhibit the growth of epithelium and decrease the number of conversion factor receptor related regulate cell apoptosis signal trans- duction, leading to excessive proliferation of gastric mucosa epithelial cells as well as related to the inactivation of tumor suppressor gene of P27.