BACKGROUND: Cyclooxygenase (COX)-2 induced by Helicobacter pylori is thought to enhance gastric carcinogenesis by affecting the maintenance of epithelial homeostasis. MATERIALS AND METHODS: Gastric biopsies from 160 subjects, 97 with nonulcer dyspepsia (47 H. pylori negative, 50 H. pylori positive) and 63 with gastric cancer were examined immunohistochemically for COX-2 expression, cell proliferation and apoptotic indices. RESULTS: COX-2 expression in corpus was significantly higher in H. pylori positive than in negative non-ulcer dyspepsia (NUD) (p <.05). Regardless of site, gastric cancer subjects had higher COX-2 expression in both antrum and corpus compared with H. pylori negative and positive NUD (p <.005). Proliferation was higher in cancer and H. pylori positive than in negative NUD (p <.0001). Moreover, cancer had enhanced proliferation than H. pylori positive NUD in corpus greater (p =.0454) and antrum lesser (p =.0215) curvatures. Apoptosis was higher in H. pylori positive than in negative NUD (p <.05). However, both had a higher index than the cancer subjects (p <.0001). Apoptosis : proliferation ratio was higher in corpus of H. pylori negative than in positive NUD in greater (p =.0122) and lesser (p =.0009) curvatures. However, both had a higher A:P ratio than cancer cases (p =.0001). A negative correlation between COX-2 expression and A:P ratio was found in corpus greater (r = -.176, p =.0437) and lesser (r = -.188, p =.0312) curvatures. CONCLUSION: The expression of COX-2 is associated with disruption in gastric epithelial kinetics and hence may play a role in gastric carcinogenesis.
BACKGROUND: Cyclooxygenase (COX)-2 induced by Helicobacter pylori is thought to enhance gastric carcinogenesis by affecting the maintenance of epithelial homeostasis. MATERIALS AND METHODS: Gastric biopsies from 160 subjects, 97 with nonulcer dyspepsia (47 H. pylori negative, 50 H. pylori positive) and 63 with gastric cancer were examined immunohistochemically for COX-2 expression, cell proliferation and apoptotic indices. RESULTS: COX-2 expression in corpus was significantly higher in H. pylori positive than in negative non-ulcer dyspepsia (NUD) (p <.05). Regardless of site, gastric cancer subjects had higher COX-2 expression in both antrum and corpus compared with H. pylori negative and positive NUD (p <.005). Proliferation was higher in cancer and H. pylori positive than in negative NUD (p <.0001). Moreover, cancer had enhanced proliferation than H. pylori positive NUD in corpus greater (p =.0454) and antrum lesser (p =.0215) curvatures. Apoptosis was higher in H. pylori positive than in negative NUD (p <.05). However, both had a higher index than the cancer subjects (p <.0001). Apoptosis : proliferation ratio was higher in corpus of H. pylori negative than in positive NUD in greater (p =.0122) and lesser (p =.0009) curvatures. However, both had a higher A:P ratio than cancer cases (p =.0001). A negative correlation between COX-2 expression and A:P ratio was found in corpus greater (r = -.176, p =.0437) and lesser (r = -.188, p =.0312) curvatures. CONCLUSION: The expression of COX-2 is associated with disruption in gastric epithelial kinetics and hence may play a role in gastric carcinogenesis.