Helicobacter pylori Eradication Prevents Extension of Intestinalization Even in the High-Risk Group for Gastric Cancer

Background/Aims: CDX2 is associated with the intestinal phenotype in the gastrointestinal tracts and is expressed in the intestinal type of gastric cancer. Helicobacter pylori-associated atrophic gastritis is characterized by aberrant expression of CDX2. The aim was to investigate the effects of era...

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Published inDigestion Vol. 81; no. 4; pp. 223 - 230
Main Authors Shiotani, Akiko, Nishi, Ryuji, Uedo, Noriya, Iishi, Hiroyasu, Tsutsui, Hideaki, Ishii, Manabu, Imamura, Hiroshi, Kamada, Tomoari, Hata, Jiro, Haruma, Ken
Format Journal Article
LanguageEnglish
Published Basel, Switzerland S. Karger AG 01.01.2010
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Summary:Background/Aims: CDX2 is associated with the intestinal phenotype in the gastrointestinal tracts and is expressed in the intestinal type of gastric cancer. Helicobacter pylori-associated atrophic gastritis is characterized by aberrant expression of CDX2. The aim was to investigate the effects of eradication to the expression of genes related to the gastric and intestinal phenotype including CDX2. We compared the effect of eradication between the patients at high risk for gastric cancer and controls. Methods: 20 patients with endoscopic resection for early gastric cancer and 12 sex- and age-matched controls were studied. CDX2 and mucin mRNA expressions were examined using whole biopsy specimens and microdissected gastric glands taken from corpus lesser and greater curves before and 1 year after eradication. Results:CDX2 and MUC2 expressions in the cancer group were significantly higher than in the controls and were significantly decreased after eradication. MUC5AC (p = 0.01) and MUC6 (p = 0.02) expression significantly increased in the control group; the difference between the two groups became significant after eradication. CDX2 expression in the glands without goblet cells was detectable and disappeared after eradication. Conclusion:H. pylori eradication can reverse gastric phenotype and diminish aberrant CDX2 expression in the early stage of intestinalization.
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ISSN:0012-2823
1421-9867
DOI:10.1159/000264651