Zali Mohammad Reza, Moaven Omeed, Asadzadeh Aghdaee Hamid, Ghafarzadegan Kamran, Ahmadi Khadijeh Jami, Farzadnia Mehdi, Arabi Azadeh, Abbaszadegan Mohammad Reza
Research Center for Gastroenterology and Liver Disease (RCGLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.
J Res Med Sci. 2009 Jul;14(4):239-47.
E-cadherin/catenin complexes exert a role in cell adhesion. β-catenin is a key player in Wnt signaling pathway in gastric cancer. P53 is a tumor suppressor gene which also regulates apoptosis. We assessed the expression of E-cadherin, β-catenin and p53 in gastric adenocarcinoma, and their correlations with clinicopathological features.
Fifty six formalin-fixed, paraffin-embedded archival specimens of gastric adenocarcinoma were randomly included as cases. Adjacent tumor-free gastric mucosa of different premalignant stages was obtained from the cases. Immunohistochemical staining was performed to assess E-cadherin, β-catenin and p53 expression.
All chronic atrophic gastritis and intestinal metaplasia revealed normal membranous staining. Only one patient with dysplasia had abnormal expression of E-cadherin and β-Catenin. Abnormal E-cadherin, β-catenin and p53 expression was found in 50%, 48.2% and 76.8% of cancer specimens respectively. Abnormal expression of E-cadherin was significantly correlated with aberrant β-catenin expression. Abnormal E-cadherin and β-catenin expression were significantly correlated with depth of tumor invasion and advanced gastric cancer (p < 0.05), lower degree of differentiation and diffused tumor type (p < 0.001). Node metastasis was not influenced by abnormal expression of E-cadherin and β-catenin. P53 was not associated with clinicopathological variables.
Abnormal expression of the E-cadherin and β-catenin were associated with each other and influenced by histogenesis of gastric cancer and malignant behavior of tumor but not significant in premalignant lesions. They are more frequent in diffuse type and associated with advanced gastric cancer. P53 alterations are more frequent in the Iranian population compared with others.
E-钙黏蛋白/连环蛋白复合物在细胞黏附中发挥作用。β-连环蛋白是胃癌中Wnt信号通路的关键因子。P53是一种肿瘤抑制基因，也调节细胞凋亡。我们评估了E-钙黏蛋白、β-连环蛋白和P53在胃腺癌中的表达及其与临床病理特征的相关性。
随机选取56例福尔马林固定、石蜡包埋的胃腺癌存档标本作为病例。从这些病例中获取不同癌前阶段的相邻无肿瘤胃黏膜。采用免疫组织化学染色评估E-钙黏蛋白、β-连环蛋白和P53的表达。
所有慢性萎缩性胃炎和肠化生均显示正常的膜染色。仅1例发育异常患者E-钙黏蛋白和β-连环蛋白表达异常。分别在50%、48.2%和76.8%的癌标本中发现E-钙黏蛋白、β-连环蛋白和P53表达异常。E-钙黏蛋白表达异常与β-连环蛋白异常表达显著相关。E-钙黏蛋白和β-连环蛋白表达异常与肿瘤浸润深度和进展期胃癌显著相关（p<0.05），与低分化程度和弥漫型肿瘤类型显著相关（p<0.001）。淋巴结转移不受E-钙黏蛋白和β-连环蛋白异常表达的影响。P53与临床病理变量无关。
E-钙黏蛋白和β-连环蛋白的异常表达相互关联，受胃癌组织发生和肿瘤恶性行为影响，但在癌前病变中不显著。它们在弥漫型中更常见，与进展期胃癌相关。与其他人群相比，伊朗人群中P53改变更为频繁。
