An Inverse Relationship between the Expression of the Gastric Tumor Suppressor RUNX3 and Infection with Helicobacter pylori in Gastric Epithelial Dysplasia.
- Author:
Woo Chul CHUNG
1
;
Sung Hoon JUNG
;
Kyu Re JOO
;
Min Ji KIM
;
Gun Jung YOUN
;
Yaeni KIM
;
Joune Seup LEE
;
Hyewon LEE
;
Ji Han JUNG
;
Yun Kyung LEE
Author Information
1. Department of Internal Medicine, St. Vincent's Hospital, The Catholic University of Korea College of Medicine, Suwon, Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
CagA protein;
Core binding factor alpha 3 subunit
- MeSH:
Adenoma/*chemistry;
Aged;
Antigens, Bacterial/genetics;
Bacterial Proteins/genetics;
Carcinoma/*chemistry;
Cell Transformation, Neoplastic;
Core Binding Factor Alpha 3 Subunit/*analysis;
Female;
Gastric Mucosa/*chemistry/pathology;
Helicobacter Infections/*metabolism;
Helicobacter pylori/*genetics;
Humans;
Male;
Middle Aged;
Mucin 5AC/analysis;
Mucin-2/analysis;
Mucin-6/analysis;
Neprilysin/analysis;
Phenotype;
Precancerous Conditions/*chemistry/pathology;
Stomach Neoplasms/*chemistry
- From:Gut and Liver
2013;7(6):688-695
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: This study was performed to determine the association between RUNX3 expression and Helicobacter pylori infection in premalignant gastric lesions. METHODS: We examined 107 patients with gastric epithelial dysplasia who had undergone endoscopic mucosal resection or submucosal dissection. All tissue samples were evaluated by RUNX3 staining and subclassified by immunophenotype. H. pylori infection in dysplastic lesions and the normal surrounding tissue was examined by silver staining, and cagA status was assessed by polymerase chain reaction. RESULTS: The loss of RUNX3 expression was observed in 62 cases (57.9%), and an association with H. pylori infection was found in 54 cases (50.5%). The infection rate with the cagA-positive H. pylori strain was 63.0%. In RUNX3-negative lesions, the rate of H. pylori infection (p=0.03) and the frequency of category 4 lesions (according to the revised Vienna classification) were high (p=0.02). In addition, the gastric mucin phenotype was predominant. In RUNX3-negative category 4 lesions, the rate of cagA-positive H. pylori infection rate was high but not significantly increased (p=0.08). CONCLUSIONS: Infection with H. pylori is associated with inactivation of RUNX3 in early gastric carcinogenesis. This mechanism was prominent in gastric cancer with a gastric mucin phenotype.
