AIM: To explore the association of p53-MDM2 feedback loop related proteins with gastric pathologies in relation to Helicobacter pylori infection. METHODS: Gastric biopsies were obtained from 157 H. pylori-negative and positive patients, including normal gastric mucosa (NGM), chronic gastritis (CG), intestinal metaplasia (IM), dysplasia (Dys), and gastric cancer (GC). The expression of mutant p53, MDM2, Bax and PUMA in gastric tissues was detected by immunohistochemistry. RESULTS: Overall expression of MDM2 and Bax is progressively increased from NGM to GC. PUMA expression is increased in CG but subsequently decreased after the development of IM. H. pylori infection is associated with increased mutant p53 and Bax expression but decreased PUMA expression in IM, and increased MDM2 expression in Dys. CONCLUSIONS: These results suggest that different p53-MDM2 feedback loop related proteins are distinctly expressed in the various stages of gastric carcinogenesis; their roles in gastric carcinogenesis in the presence of H. pylori infection need to be further investigated.
AIM: To explore the association of p53-MDM2 feedback loop related proteins with gastric pathologies in relation to Helicobacter pylori infection. METHODS: Gastric biopsies were obtained from 157 H. pylori-negative and positive patients, including normal gastric mucosa (NGM), chronic gastritis (CG), intestinal metaplasia (IM), dysplasia (Dys), and gastric cancer (GC). The expression of mutant p53, MDM2, Bax and PUMA in gastric tissues was detected by immunohistochemistry. RESULTS: Overall expression of MDM2 and Bax is progressively increased from NGM to GC. PUMA expression is increased in CG but subsequently decreased after the development of IM. H. pylori infection is associated with increased mutant p53 and Bax expression but decreased PUMA expression in IM, and increased MDM2 expression in Dys. CONCLUSIONS: These results suggest that different p53-MDM2 feedback loop related proteins are distinctly expressed in the various stages of gastric carcinogenesis; their roles in gastric carcinogenesis in the presence of H. pylori infection need to be further investigated.