Clinicopathological significance of E-cadherin, β-catenin and p53 expression in gastric adenocarinoma

BACKGROUND: E-cadherin/catenin complexes exert a role in cell adhesion. beta-catenin is a key player in Wilt signaling pathway in gastric cancer. P53 is a turner Suppressor gene which also regulates apoptosis. We assessed the expression of E-cadherin, beta-catenin and p53 in gastric adenocarcinoma, and their correlations with clinicopathological features. METHODS: 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, beta-catenin and p53 expression. RESULTS: All chronic atrophic gastritis and intestinal metaplasia revealed normal membranous staining. Only one patient with dysplasia had abnormal expression of E-cadherin and beta-catenin. Abnormal F-cadherin. beta-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 beta-catenin expression. Abnormal E-cadherin and beta-catenin expression were significantly correlated with depth of turner 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 P-catenin. P53 was not associated with clinicopathological variables. CONCLUSIONS: Abnormal expression of the E-cadherin and beta-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.