BACKGROUND/AIMS: Reduced expression of E-cadherin leading to loss of cellular adhesion is crucial for cancer invasion and metastasis. The aim of this study is to investigate the role of E-cadherin in gastric tumorigenesis. METHODOLOGY: Immunohistochemical expression of E-cadherin was analyzed and correlated with clinicopathological characteristics of 122 patients with gastric cancer. RESULTS: Reduced E-cadherin expression was noted in 71 tumors (58.2%), while all normal epithelium showed a normal expression. Correlation of E-cadherin status to histological subtypes and growth patterns revealed a significantly higher frequency of reduced expression in diffuse type (46/60, 76.7%), advanced tumors (48/68, 70.6%) and stage III/IV (39/53, 73.6%) than that in intestinal type (25/62, 40.3%, p<0.0001), early tumors (23/54, 42.6%, p<0.005) and stage I/II (32/69, 46.4%, p<0.005) respectively. Moreover, abnormal expression was more frequent in tumors with positive lymph node metastasis (45/62, 72.6%), peritoneum seeding (10/11, 90.9%) and venous permeation (27/37, 73%) than that in tumors without lymph node metastasis (26/60, 43.3%, p<0.005), peritoneum seeding (61/111, 55.0%, p<0.05) and venous permeation (44/85, 51.8%, p<0.05). There is no statistical difference between E-cadherin expression and the status of perineural invasion or H. pylori infection. Analysis of survival for patients demonstrated that reduced E-cadherin expression was correlated with poor prognosis. CONCLUSIONS: These data indicate that impaired expression of E-cadherin is an important characteristic of gastric cancer and contributes to histogenesis, tumor growth, metastasis and poor survival.
BACKGROUND/AIMS: Reduced expression of E-cadherin leading to loss of cellular adhesion is crucial for cancer invasion and metastasis. The aim of this study is to investigate the role of E-cadherin in gastric tumorigenesis. METHODOLOGY: Immunohistochemical expression of E-cadherin was analyzed and correlated with clinicopathological characteristics of 122 patients with gastric cancer. RESULTS: Reduced E-cadherin expression was noted in 71 tumors (58.2%), while all normal epithelium showed a normal expression. Correlation of E-cadherin status to histological subtypes and growth patterns revealed a significantly higher frequency of reduced expression in diffuse type (46/60, 76.7%), advanced tumors (48/68, 70.6%) and stage III/IV (39/53, 73.6%) than that in intestinal type (25/62, 40.3%, p<0.0001), early tumors (23/54, 42.6%, p<0.005) and stage I/II (32/69, 46.4%, p<0.005) respectively. Moreover, abnormal expression was more frequent in tumors with positive lymph node metastasis (45/62, 72.6%), peritoneum seeding (10/11, 90.9%) and venous permeation (27/37, 73%) than that in tumors without lymph node metastasis (26/60, 43.3%, p<0.005), peritoneum seeding (61/111, 55.0%, p<0.05) and venous permeation (44/85, 51.8%, p<0.05). There is no statistical difference between E-cadherin expression and the status of perineural invasion or H. pyloriinfection. Analysis of survival for patients demonstrated that reduced E-cadherin expression was correlated with poor prognosis. CONCLUSIONS: These data indicate that impaired expression of E-cadherin is an important characteristic of gastric cancer and contributes to histogenesis, tumor growth, metastasis and poor survival.