https://scholars.lib.ntu.edu.tw/handle/123456789/545353
標題: | Compartment theory in Helicobacter pylori-associated gastric carcinogenesis | 作者: | Tseng H.-H. Hsu P.-I. Chen H.-C. Lai K.-H. Lo G.-H. Lo C.-C. Chou N.-H. Mok K.-T. Chen I.-S. Chou N.-H. Yang H.-B. Liu L. PING-NING HSU |
關鍵字: | Compartment; Gastric cancer; Gastritis; Growth kinetics; Helicobacter pylori; Intestinal metaplasia | 公開日期: | 2003 | 卷: | 23 | 期: | 4 | 起(迄)頁: | 3223-3229 | 來源出版物: | Anticancer Research | 摘要: | Background: The compartment theory has not been well investigated in gastric carcinogenesis. This study was aimed at examining the compartment alterations through the Helicobacter pylori (H. pylori)-related chronic gastritis-intestinal metaplasia -carcinoma sequence, and investigating the long-term effect of bacterial eradication on the compartment changes. Patients and Methods: Gastric biopsy specimens were obtained from subjects with H. pylori-negative normal mucosa (N=12), H. pylori-positive non-metaplastic gastritis (N=42), H. pylori-positive intestinal metaplasia (N=21) and intestinal-type adenocarcinoma (N=20). The specimens were immnostained for monocloncal antibodies against the proliferating cell nuclear antigen (PCNA) for proliferating analysis. Additionally, 50 patients with H. pylori-positive gastritis were enrolled to investigate the long-term effect of bacterial eradication on the compartment changes of gastric epithelium. Results: The mean PCNA labeling indices (L.I.) of non-metaplastic gastritis, intestinal metaplasia and adenocarcinoma were significantly higher than that of normal mucosa (31.1, 49.2 and 40.7 vs. 21.4; p <0.01, 0.001 and 0.001, respectively). The proliferating zone was principally located in the lower compartment of normal mucosa. In patients with intestinal metaplasia, there was a full expansion (phase I change) of proliferating zone to the middle compartment of gastric pits (ratio of L.I. between middle and lower compartment = 1.00). The proliferating cells were evenly distributed in adenocarcinoma (complete loss of compartmentalization). Eradiation of H. pylori led to a reversion of compartment changes of gastric epithelium in patients with chronic gastritis. Conclusion: H. pylori-related gastric carcinognesis is a multistep process involving progressive alterations of proliferating activity as well as loss of compartmentalization. Eradication of H. pylori reverses the changes in growth kinetics of gastric epithelium. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0042029383&partnerID=40&md5=f198e771096997bb796e733929b3485d https://scholars.lib.ntu.edu.tw/handle/123456789/545353 |
ISSN: | 0250-7005 | SDG/關鍵字: | cycline; monoclonal antibody; adenocarcinoma; adult; article; bacterial infection; cancer growth; carcinogenesis; cell proliferation; chronic gastritis; controlled study; disease association; eradication therapy; female; Helicobacter pylori; histopathology; human; human tissue; immunohistochemistry; intestine carcinoma; intestine metaplasia; major clinical study; male; nonhuman; priority journal; statistical significance; stomach carcinoma; stomach epithelium; stomach mucosa; 2-Pyridinylmethylsulfinylbenzimidazoles; Adenocarcinoma; Aged; Cell Cycle; Cell Division; Chronic Disease; Disease Progression; Drug Therapy, Combination; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Metronidazole; Middle Aged; Omeprazole; Stomach Neoplasms; Tetracycline |
顯示於: | 醫學系 |
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