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KMID : 0876319990010020113
Cachon Medical Journal
1999 Volume.1 No. 2 p.113 ~ p.119
Helicobacter pylori Infection and Expression of CagA in Patients with Gastric Cancer
Kang Dong-Hoon

Hwang Yu-Jin
Park Dong-Kyun
Yoo Jong-Hyeon
Park Hyun-Chul
Ha Seung-Yeon
Lee Woon-Gi
Kim Ju-Hyun
Abstract
Purpose: H. pylori infection is an important risk factor for the development of gastric cancer. Gastric adenocarcinoma is resistant to H. pylori colonization even when the rest of stomach is colonized, because cancer tissue lacks a factor necessary for colonization of H. pylori. The detection of H. pylori in gastric cancer depends on the diagnostic tests, specimen used, and handling of specimen. Intestinal metaplasia is thought by some investigators to be linked to intestinal carcinoma. It could results from long-standing gastric inflammation due to H. pylori. The aims of this study are 1) to compare infection rates of H. pylori between cancer and normal tissues of gastric cancer using
gastrectomy specimen and 2) to compare H. pylori infection in gastric cancer and cagA expression in H. pyzori infected gastric cancer according to histopathologic classification.
Materials and Methods: Cancer and normal tissues from resected stomach in 31 patients with advanced gastric cancer were tested. PCR for H. pylori infection using the primers of 109 bp sized 165 rRNA and 159 bp sized Unease B gene was performed. RT-PCR for cagA expression was also performed in H. pylori infected gastric cancer. H. pylori infection and cagA expression were compared between diffuse and intestinal types of gastric cancer.
Results: H. pylori was detected in 28(90.3%) of 31 gastrectomy specimen of gastric cancer by PCR and detected in 26(83.9%) of normal tissue and 15(48.4%) of cancer tissue. H. pylori was detected in 23(74.2%) of normal tissue and 2(6.5%) of cancer tissue by H&E stain after conventional gastrectomy preparation. H. pylori was detected in 92.9% of intestinal, 81.8% of diffuse, and 100% of mixed type adenocarcinoma. CagA was expressed in 21 (75.0%) of 28 H. pylori infected gastric cancers. Four (14.3%) H. pylori infected gastric cancers showed different expressions in cancer and normal tissue of same patients. CagA was expressed in 76.9% of intestinal, 75% of diffuse, and 7l.4% of mixed type adenocarcinomas.
Conslusions: The detection of H. pylori was higher in normal tissue than in cancer tissue of gastrectomy specimens. H. pylori infection and cagA expression were not different among the intestinal, diffuse, and mixed types in advanced gastric cancer.
KEYWORD
CagA, Histopathology, Helicobacter pylori, PCR, Stomach cancer
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