Loss of Fas Expression in Gastric Cancer:Correlation with Clinicopathologic Parameters

Background/Aims: The Fas-FasL system is the main pathway for the induction of apoptosis in normal and malignant tumor cells. The binding of FasL in the cytotoxic T lymphocytes or Anti-Fas antibody to Fas receptor in cell membrane induces apoptosis. Loss of Fas expression has been demonstrated in a variety of tumor cells. Recently, it is reported that gastric cancers express Fas ligand and downregulate Fas to escape from the host immune surveillance. Methods: We performed clinicopathological and immunohistochemical studies for Fas, FasL, P53, E-cadherin, beta-catenin, and Ki-67 in the specimens obtained from 52 gastric cancer patients treated with curative resections from 2000 to 2002. Results: Loss of Fas and expression of FasL were observed in 15 (28.8%) and 19 (36.5%) patients respectively. The loss of Fas expression was dominantly demonstrated in poorly differentiated and diffuse type of gastric carcinoma. Loss of Fas expression had a significant correlation with nuclear expression of beta-catenin (p=0.027). Conclusions: Loss of Fas expression in gastric cancer is significantly influenced by histological grade, Lauren classification, and nuclear expression of beta-catenin. These findings indicate that loss of Fas expression correlates with aggressiveness of gastric cancer.