Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2009
Clinicopathological significance of E-cadherin, β-catenin and p53 expression in gastric adenocarinoma.
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Zali Mohammad Reza, Moaven Omeed, Asadzadeh Aghdaee Hamid, Ghafarzadegan Kamran, Ahmadi Khadijeh Jami, Farzadnia Mehdi, Arabi Azadeh, Abbaszadegan Mohammad Reza
Аннотация
BACKGROUND: 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.
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, β-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 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.
CONCLUSIONS: 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.
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, β-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 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.
CONCLUSIONS: 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.