Helicobacter pylori infection and relationship with gastric epithelial cell proliferation and apoptosis

To evaluate the effects of Helicobacter pylori on cell proliferation and apoptosis in gastric cancer (GC) both at tumoral and nontumoral sites and in gastritis. Materials and methods: Biopsies from 96 patients (gastric cancer = 52, gastritis = 44) were examined immunohistochemically and histopathologically. Results: In H. pylori-positive GC patients the average proliferative index (PI) in tumor and nontumor sites was 40.7% and 24.8%, while in H. pylori-negative patients it was 32.9% and 17.8%, respectively. The PI was significantly higher in the tumor than in the nontumor sites, regardless of H. pylori infection. Cell proliferation was also significantly associated with intestinal metaplasia in nontumor sections. The apoptotic index (AI) in H. pylori-positive GC tumor and nontumor sites showed an average of 61.8% and 50.0%, while in H. pylori-negative patients it was 38.1% and 25.0%, respectively. The AI was significantly higher in both groups in the presence of H. pylori. In gastritis, H. pylori infections lead to a significantly higher PI than AI. H. pylori infection increased the PI and the AI in cases of GC. Conclusion: H. pylori induced higher proliferative and apoptotic activities in both tumor and nontumor sites of the GC sections, a fact that provides supportive evidence for its effect.

Helicobacter pylori infection and relationship with gastric epithelial cell proliferation and apoptosis

To evaluate the effects of Helicobacter pylori on cell proliferation and apoptosis in gastric cancer (GC) both at tumoral and nontumoral sites and in gastritis. Materials and methods: Biopsies from 96 patients (gastric cancer = 52, gastritis = 44) were examined immunohistochemically and histopathologically. Results: In H. pylori-positive GC patients the average proliferative index (PI) in tumor and nontumor sites was 40.7% and 24.8%, while in H. pylori-negative patients it was 32.9% and 17.8%, respectively. The PI was significantly higher in the tumor than in the nontumor sites, regardless of H. pylori infection. Cell proliferation was also significantly associated with intestinal metaplasia in nontumor sections. The apoptotic index (AI) in H. pylori-positive GC tumor and nontumor sites showed an average of 61.8% and 50.0%, while in H. pylori-negative patients it was 38.1% and 25.0%, respectively. The AI was significantly higher in both groups in the presence of H. pylori. In gastritis, H. pylori infections lead to a significantly higher PI than AI. H. pylori infection increased the PI and the AI in cases of GC. Conclusion: H. pylori induced higher proliferative and apoptotic activities in both tumor and nontumor sites of the GC sections, a fact that provides supportive evidence for its effect.

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Turkish Journal of Medical Sciences-Cover
  • ISSN: 1300-0144
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
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