Expression of p27(Kip1) in gastric cancers and precancerous lesions / 대한내과학회지

BACKGROUND: The cyclin-dependent kinase inhibitor p27(Kip1) is a negative regulator of cell cycle progression at G1/S transition. Recently, the expression level of p27(Kip1) was decreased in many cancers such as breast, pituitary gland, colon and stomach. We studied the expression of p27(Kip1) in gastric cancers, precancerous lesions and normal gastric tissues and analysed its correlation to clinicopathologic data including tumor differentiation, tumor depth, nodal and distant metastasis in gastric cancers. METHODS: p27(Kip1) were immunohistochemically stained in the tissue specimens of 62 resected cancers, 110 corresponding adjacent non-neoplastic tissues, 22 gastric adenomas and 10 normal gastric tissues. Adjacent non-neoplastic tissues consisted of 32 chronic gastritis, 29 intestinal metaplasia and 49 transitional mucosa. RESULTS: Gastric cancers showed significantly decreased expression level of p27(Kip1) when compared with non-neoplastic lesions and adenomas. Labeling index of p27(Kip1) were more decreased in chronic gastritis, intestinal metaplasia and transitional mucosa than in normal mucosa. Early gastric cancers showed significantly decreased expression level of p27(Kip1) when compared with advanced gastric cancers. In gastric cancers, p27(Kip1) labeling index was significantly decreased in diffuse type and presence of nodal metastasis however did not show relationship with distant metastasis and tumor depth of advanced gastric cancers. CONCLUSION: We suggest that p27(Kip1) may be decreased in the early stage of gastric carcinogenesis and play an important role in the progression and differentiation of gastric cancers. More further studies are thought to be necessary in order to evaluate its prognostic factor in gastric cancers.

Effect of Helicobacter pylori eradication on proliferation and apoptosis of gastric epithelial cells / 대한내과학회지

Helicobacter pylori (H. pylori) is the principle cause of type B gastritis and peptic ulcer disease and has been classified as group I carcinogen for gastric cancer. H. pylori may affect the normal balance between gastric cell proliferation and epithelial cell death, thus interfering with the maintenance of gastric mucosal integrity. The aim of this study was to investigate the effect of H. pylori on cell proliferation and apoptosis according to the effect of eradication of H. pylori. METHODS: The subjects were 45 patients who had undergone diagnostic gastroduodenoscopy; 11 with gastritis, seven with gastric ulcer and 27 duodenal ulcer. H. pylori infection was assessed by H&E and immunohistochemical stain with anti-H. pylori polyclonal antibody and rapid urease test. Acute and chronic inflammation, apoptosis and intestinal metaplasia were scored according to the updated Sydney system. Gastric epithelial cell proliferation was assessed by immunohostochemical method using Ki-67 monoclonal antibody. In situ apoptosis was detected with in situ terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling. RESULTS: Acute and chronic inflammation, intestinal metaplasia, Ki-67 labeling index, and apoptosis were significantly higher in H. pylori infected persons (n=45) than in uninfected persons (n=5)(p<0.05). Acute and chronic inflammation, intestinal metaplasia, Ki-67 labeling index and apoptosis in H. pylori eradicated group (n=25) significantly decreased after eradication therapy (p<0.05), but no significant differences of them was observed in H. pylori non-eradicated goup (n=20) after eradication therapy. Ki-67 labeling index was significantly correlated with acute inflammation, chronic inflammation and apoptosis (p<0.05). Apoptosis was significantly correlated with acute and chronic inflammation (p<0.05). CONCLUSION: In eradicated group, epithelial apoptosis and proliferation closely associated with gastric carcinogenesis are stabilized after treatment, which suggests H. pylori eradication therapymay preven the early step of gastric carcinogenesis.