Romiti Adriana, Zullo Angelo, Borrini Francesco, Sarcina Ida, Hassan Cesare, Winn Simon, Tomao Silverio, Vecchione Aldo, Morini Sergio, Mingazzini Pietro
Medical Oncology, Sant'Andrea Hospital, Rome, Italy.
World J Gastroenterol. 2005 Jul 28;11(28):4400-3. doi: 10.3748/wjg.v11.i28.4400.
To investigate beta-catenin expression in patients with intestinal metaplasia, and to look for a possible relationship between beta-catenin expression and either epithelial proliferation values or Helicobacter pylori (H pylori) infection.
Twenty patients with complete type intestinal metaplasia were studied. beta-Catenin expression and epithelial cell proliferation in antral mucosa were assessed using an immunohistochemical analysis. H pylori infection was detected by histology and a rapid urease test.
Reduced beta-catenin expression on the surface of metaplastic cells was detected in 13 (65%) out of 20 patients. Moreover, in eight (40%) patients intranuclear expression of beta-catenin was found. When patients were analyzed according to H pylori infection, the prevalence of both beta-catenin reduction at the cell surface and its intranuclear localization did not significantly differ between infected and uninfected patients. Cell proliferation was higher in patients with intranuclear beta-catenin expression as compared to the remaining patients, although the difference failed to reach the statistical significance (36+/-8.9 vs 27.2+/-11.4, P = 0.06). On the contrary, a similar cell proliferation value was observed between patients with reduced expression of beta-catenin on cell surface and those with a normal expression (28.1+/-11.8 vs 26.1+/-8.8, P = 0.7). H pylori infection significantly increased cell proliferation (33.3+/-10.2% vs 24.6+/-7.4%, respectively, P = 0.04).
Both cell surface reduction and intranuclear accumulation of beta-catenin were detected in intestinal metaplasia. The intranuclear localization of beta-catenin increases cell proliferation. H pylori infection does not seem to play a direct role in beta-catenin alterations, whilst it significantly increases cell proliferation.
研究肠化生患者中β-连环蛋白的表达情况，并探寻β-连环蛋白表达与上皮增殖值或幽门螺杆菌（H pylori）感染之间的可能关系。
对20例完全型肠化生患者进行研究。采用免疫组织化学分析评估胃窦黏膜中β-连环蛋白的表达及上皮细胞增殖情况。通过组织学检查和快速尿素酶试验检测H pylori感染。
20例患者中有13例（65%）检测到化生细胞表面β-连环蛋白表达降低。此外，8例（40%）患者发现β-连环蛋白核内表达。根据H pylori感染情况对患者进行分析时，感染患者与未感染患者在细胞表面β-连环蛋白减少及其核内定位的发生率上无显著差异。与其余患者相比，β-连环蛋白核内表达患者的细胞增殖更高，尽管差异未达到统计学意义（36±8.9对27.2±11.4，P = 0.06）。相反，细胞表面β-连环蛋白表达降低的患者与表达正常的患者之间观察到相似的细胞增殖值（28.1±11.8对26.1±8.8，P = 0.7）。H pylori感染显著增加细胞增殖（分别为33.3±10.2%对24.6±7.4%，P = 0.04）。
在肠化生中检测到β-连环蛋白细胞表面减少和核内积聚。β-连环蛋白的核内定位增加细胞增殖。H pylori感染似乎在β-连环蛋白改变中不发挥直接作用，但其显著增加细胞增殖。
