Do Gene Expressions Differ Between Gastritis with and without Helicobacter pylori?

Objective: Helicobacter pylori infection is a well-defined risk factor for the development of gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. However, mechanisms of carcinogenesis in Helicobacter gastritis need to be elucidated. We aimed in this study to determine the immunohistochemical expressions of some cancer-associated genes, and to show differences between Helicobacter gastritis and Helicobacter-negative gastritis. Material and Methods: Sixty-three endoscopic biopsy samples were selected. The samples comprised of normal gastric mucosa (20 samples), Helicobacter gastritis (22 samples), and Helicobacter-negative gastritis (21 samples). Paraffin sections of samples were processed immunohistochemically with some suppressor genes (Rb, p53), protooncogenes (EGFR, cyclin D1), and a heat shock protein, HSP 105. The gene expressions in both crypt epithelia and lymphoid infiltrate were evaluated separately. Results: In epithelia; expressions of cyclin DI, p53, HSP 105, and EGFR were higher in Helicobacter-negative gastritis than in Helicobacter gastritis (p< 0.0001). Immune expression of HSP 105 in Helicobacter gastritis was lower than in control group (p= 0.008) as well as in Helicobacter-negative gastritis. However, expression of Rb was higher in Helicobacter gastritis than in Helicobacter-negative gastritis (p= 0.034). In lymphoid infiltrate; immune reactions for p53 and cyclin D1 were negative in all samples. Expressions of Rb, EGFR, and HSP 105 in lymphoid infiltrate were similar to expressions in epithelia for all groups. Conclusion: We can suggest that development of gastric cancer has a different pathway in Helicobacter gastritis when compared to the one Helicobacter-negative gastritis. In addition, decrease of heat shock proteins in Helicobacter gastritis may lead to sensitivity of crypt epithelia and lymphoid infiltrate for carcinogenic mutations.