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Inflammatory Bowel Diseases 09/2010; 16(9):1454-6. · 4.86 Impact Factor
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Kidney International 10/2009; 76(7):803. · 6.61 Impact Factor
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Gastroenterology 06/2009; 137(1):42, 396. · 11.68 Impact Factor
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ABSTRACT: Eradication of Helicobacter pylori appears to reduce gastric cancer incidence. We examined the effect of successful H pylori therapy on histology, phenotype of gastric intestinal metaplasia (GIM) (complete vs incomplete), and expression of several biomarkers related to carcinogenesis.
Ninety-six H pylori-positive patients from Japan were treated successfully and followed up prospectively over 4 years with yearly endoscopy and were classified into 3 groups: group CG, chronic gastritis without GIM (n = 36); group IM, chronic gastritis with GIM (n = 33); group DYS, and GIM with dysplasia/cancer in a different location of the stomach (n = 27). A total of 288 endoscopic procedures were performed. Histology, mucin-histochemistry, and immunoperoxidase assays using monoclonal antibodies (mAbs) for cell phenotype (monoclonal antibody Das-1/colonic) and for neoplasia (TC22 and p53) were performed.
The GIM histologic score was higher in group DYS than in group IM (P < .05) and group CG (P < .0001). The GIM scores did not change in groups IM and DYS over 4 years. mAb Das-1 reactivity was higher in group DYS (63%) than in group IM (39%) and group GC (0%). After eradication of H pylori, mAb Das-1 reactivity disappeared in 40% of patients (P < .0001) despite the unchanged GIM scores, and regression of TC22-4 was noted in the same patients.
H pylori eradication does not reduce the histologic GIM score, but changes the cellular phenotype of GIM. This change of phenotype may be an important factor in the reduction of cancer incidence after eradication of H pylori.
Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 05/2008; 6(4):409-17. · 5.64 Impact Factor
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ABSTRACT: Gastric intestinal metaplasia (GIM) associated with H. pylori (HP) has been considered a premalignant lesion. However, GIM phenotype associated with HP infection and gastric cancer is unclear. The expression of COX-2 in relation to GIM phenotype is also unknown.
We evaluated cellular phenotype and COX-2 expression in the GIM from HP-positive and -negative patients from Japan in the absence of gastric cancer (n = 31) by using a colon epithelium specific monoclonal antibody (mAb Das-1) and anti-COX-2 antibody. COX-2 expression was also examined in patients with gastric cancer (n = 34), both in the cancer and in the GIM areas away from the cancer field.
Sixty-eight percent of HP-positive GIM reacted with mAb Das-1, whereas the reactivity in the HP-negative GIM was only 25% (P < 0.001). The COX-2 expression was present in 32% of HP-positive GIM and in only 9% of HP-negative GIM (P < 0.001). In the cancer group, COX-2 expression was localized both in the cancer area (94%) and in the GIM (82%) away from the cancer. Each of the COX-2-positive tissue was also positive to mAb Das-1.
HP infection is highly associated with the development of colonic-phenotype of GIM, and about half of them expressed COX-2. COX-2 expression was frequent in both gastric cancer and the GIM adjacent to the cancer. The results suggest that the presence of mAb Das-1 and COX-2 reactivity in the GIM identify the subgroup of patients who may be at risk for gastric cancer and may need close surveillance.
Journal of Clinical Gastroenterology 02/2006; 40(2):122-8. · 3.16 Impact Factor
