TITLE

Apoptosis and cell proliferation are significantly affected by anatomic site and Helicobacter pylori infection of the gastric mucosa

AUTHOR(S)
Ladas, S.D.; Chatziargyriou, M.; Kitsanta, P.; Triantafyllou, K.
PUB. DATE
September 2002
SOURCE
Gut;Sep2002 Supplement 2, Vol. 51, pA42
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Introduction: Helicobacter pylori is a risk factor for gastric cancer. The association between H. pylori and cancer may be attributable to increased epithelial cell turnover. However, the underlying mechanisms and the response of different anatomic sites of the gastric mucosa to H. pylori infection remain to be defined. Aim: To investigate the apoptosis and cell proliferation rate of different anatomic sites of gastric mucosa in H. pylori +ve and -ve patients. Methods: 20 patients (M/F 10/10, age 34, 16-54 years, median, range) were studied. Six biopsies were separately obtained from the grater (GC) and lesser (LC) curvature of the antrum and corpus and the fundus and cardia. H. pylori status and cell proliferation were detected immunohistochemically with an anti-H, pylori and MIB-1 monoclonal antibodies according to the Avidin-Biotin Method. Apoptosis was measured by TUNEL method. The rate of the positive stained cells was count using image analysis technique (SABA). Results: 11 patients were H. pylori -ve and 9 +ve. Median apoptotic index was significantly different among the GC 25 and LC 20 of antrum, the GC 15 and LC 13 of corpus, the fundus 12 and the cardia 15 (P<0.001), being significantly higher at all anatomic sites in H. pylori +ve patients (P<0.001). Median proliferation index was also significantly different among the GC 2.4 and LC 3.0 of antrum, the GC 4.9 and the LC 9.2 of corpus, the fundus 10.1 and the cardia 12.8 (P<0.001). However, H. pylori +ve patients had a significantly lower proliferation index only GC (P=0.025) and LC (P=0.03) at the corpus and the cardia (P=0.04). Conclusions: Gastric cell apoptosis and proliferation are significantly affected by anatomic site and H. pylori infection, factors which are known to be related with gastric carcinogenesis.
ACCESSION #
9747517

 

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