The evaluation of tissue expression of apoptotic markers bcl-2 and cox-2, apoptosis and proliferation in patients with intestinal metaplasia

Intestinal metaplasia (IM) is the replacement of gastric mucosa with epithelium that resembles the mucosa of the small intestine. It is classified as complete (Type I) and incomplete (Type II and Type III) according to Jass and Filipe. The risk of gastric cancer is incrased ten fold in patients with intestinal metaplasia. Apoptosis is defined as programmed cell death. In our study, an increase in apoptosis was not observed in patients with IM when compared to patients with chronic active gastritis or normal gastric mucosa. Ki-67 is a marker of proliferation. We demonstrated a statistically significant increase in proliferation with Ki-67 staining in patients with IM when compared to chronic active gastritis. Bcl-2 is an antiapoptotic protooncogene, the overproduction of which results in prolonged cell life span despite apoptotic stimuli. We did not observe an increase in Bcl-2 expression in patients with IM. Cox-2 is the key enzyme that catalyses the synthesis of prostoglandins and other eicasanoids from arachidonic acid. We found that the frequency and magnitude of Cox-2 expression is statistically significantly higher in patients with IM when compared to patients with chronic active gastritis. As a conclusion, we found that the expressions of Ki-67 and Cox-2 are increased in patients with IM when compared to patients with chronic active gastritis and normal mucosa. On the other hand, there is no significant difference in apoptosis and Bcl-2 expression. We hypothesized that constant apoptosis despite increase in proliferation and the increase of antiapoptotic Cox-2 expression may stimulate gastric carcinogenesis.