Expression of cyclooxygenase-2 and nitrotyrosine in human gastric mucosa before and after Helicobacter pylori eradication

Kimura, Atsuomi; Tsuji, S.; Tsujii, Masahiko; Sawaoka, Hitoshi; Iijima, Hideki; Kawai, Naoki; Yasumaru, Masakazu; Kakiuchi, Yohei; Okuda, Yoshinobu; Ali, Z. A. G. M.; Nishimura, Y; Sasaki, Yutaka; Kawano, Seiji; Hori, Masatsugu

doi:10.1054/plef.2000.0220

Cited by 25 publications

(18 citation statements)

References 41 publications

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“…Furthermore, high expression levels of COX-2 in intestinal metaplasia have been observed even after H. pylori eradication. 47 Treatment with a selective COX-2 inhibitor thus appears to represent a reasonable option for subjects with metaplastic gastritis, rather than regular follow-up for cancer.…”

Section: Discussionmentioning

confidence: 99%

Preventive effects of etodolac, a selective cyclooxygenase‐2 inhibitor, on cancer development in extensive metaplastic gastritis, a Helicobacter pylori‐negative precancerous lesion

Yanaoka

Oka

Yoshimura

et al. 2009

Intl Journal of Cancer

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The present study investigated the preventive effects of etodolac, a selective cyclo-oxygenase (COX)-2 inhibitor, on metachronous cancer development after endoscopic resection of early gastric cancer. Among 267 early gastric cancer patients who underwent endoscopic resection, 47 patients with extensive metaplastic gastritis were selected based on endoscopic findings and our previously described criteria of serum pepsinogen (PG) test-positive and Helicobacter pylori antibodynegative conditions. Nonrandomized etodolac treatment (300 mg/day) was administered to 26 patients (Group A), while the remaining 21 patients were untreated (Group B). No significant differences in age, sex distribution, lifestyle factors or extent of metaplastic gastritis at baseline were identified between groups. Patients were followed for metachronous cancer development with endoscopy every 6-12 months for up to 5 years. Mean (standard deviation) follow-up period was 4.2 (0.9) years. In Group B, 5 cancers developed (incidence rate 5 6,266/100,000 person-years), significantly more than the 1 cancer in Group A (incidence rate 5 898/100,000 person-years; p < 0.05). Long-term etodolac treatment did not influence the extent of metaplastic gastritis as revealed by endoscopic findings or by serum PG levels, but effectively reduced metachronous cancer development in patients with extensive metaplastic gastritis. These results strongly suggest that chemoprevention of cancer in the metaplastic stomach is possible by controlling COX-2 expression.Helicobacter pylori triggers chronic inflammation of the infected stomach mucosa and is considered a major risk factor for gastric cancer and associated precursor lesions. 1 As postulated in the multistep model of gastric cancer development by Correa, long-lasting inflammation in the stomach mucosa leads to a cascade of molecular and morphological changes of stomach carcinogenesis, representing the gastritisatrophy-metaplasia-dysplasia-cancer sequence. 2 This sequence of stomach carcinogenesis is now widely accepted to be strongly promoted by H. pylori and is affected by a variety of genetic and environmental factors that may act synergistically. 3 H. pylori eradication thus appears to be the most promising approach for the control of gastric cancer development, and the results of animal experiments have revealed that eradication of H. pylori, especially in the early stage, is effective for preventing stomach carcinogenesis. [4][5][6] However, current data indicate that H. pylori eradication does not lead to complete eradication of gastric cancer 7-12 and might be effective only in subjects without chronic atrophic gastritis (CAG) together with intestinal metaplasia. 7,10 Moreover, patients with extensive intestinal metaplasia-that is, metaplastic gastritis-should not be treated with eradication

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Section: Discussionmentioning

confidence: 99%

Preventive effects of etodolac, a selective cyclooxygenase‐2 inhibitor, on cancer development in extensive metaplastic gastritis, a Helicobacter pylori‐negative precancerous lesion

Yanaoka

Oka

Yoshimura

et al. 2009

Intl Journal of Cancer

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“…Specifically, H. pylori-related gastritis has been seen to induce its expression depending upon bacterial strain (113,(115)(116)(117)(118)(119)(120)(121)(122)(123), which may partly explain its distinct pathogenic potential (123,124). Infection by H. pylori cagA + strains has been seen to overexpress COX-2 in patients with gastric cancer (123).…”

Section: Changes In the Expression Of Enzymes Related To Inflammationmentioning

confidence: 99%

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Olivares

Gisbert

2005

Rev. esp. enferm. dig.

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“…23 The second histological type, the dif- Mucosal COX-2 expression has been shown to continue in patients with IM, even after eradication of H. pylori infection. 26 Other investigators have found that patients with IM exhibited reduced COX-2 expression at 1 year after successful H. pylori eradication, compared to expression before eradication therapy.…”

Section: Discussionmentioning

confidence: 96%

Helicobacter pyloriEradication Suppresses Metachronous Gastric Cancer and Cyclooxygenase-2 Expression after Endoscopic Resection of Early Gastric Cancer

Kim

Hong

et al. 2011

Korean J Helicobacter Up Gastrointest Res

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Background/Aims: The impact of Helicobacter pylori (H. pylori) eradication after endoscopic resection (ER) of early gastric cancer (EGC) has not been fully evaluated. We tried to find out the effect of H. pylori eradication therapy on the development of metachronous gastric cancers and changes in Cyclooxygenase-2 (COX-2) expression following attempts to eradicate H. pylori after ER of EGC. Materials and Methods: We eradicated H. pylori in the patients with EGC after ER. Biopsy samples were taken according to the follow-up schedules for surveillance after ER. Results: Fifty five patients were enrolled and finished the follow up schedules. Of the 55, 28 were successfully treated H. pylori infection, and the other 27 were failed eradication of H. pylori. The mean follow-up period was 60.8 months. Five in the H. pylori ongoing infection group developed metachronous gastric cancer, whereas no new gastric cancers were found in the 28 eradication group (P=0.023). COX-2 expression in the eradication group was significantly decreased (1.4±0.2, n=28), compared to that in H. pylori ongoing infection group (3.0±0.4, n=27, P=0.0001) after the follow-up. Conclusions: The eradication of H. pylori seems to have a preventative effect on the development of metachronous adenocarcinomas and a suppressive effect on COX-2 expression in the patients after ER for EGC. (Korean J Helicobacter Upper Gastrointest Res 2011;11:117-123)

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Expression of cyclooxygenase-2 and nitrotyrosine in human gastric mucosa before and after Helicobacter pylori eradication

Cited by 25 publications

References 41 publications

Preventive effects of etodolac, a selective cyclooxygenase‐2 inhibitor, on cancer development in extensive metaplastic gastritis, a Helicobacter pylori‐negative precancerous lesion

Preventive effects of etodolac, a selective cyclooxygenase‐2 inhibitor, on cancer development in extensive metaplastic gastritis, a Helicobacter pylori‐negative precancerous lesion

Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Helicobacter pyloriEradication Suppresses Metachronous Gastric Cancer and Cyclooxygenase-2 Expression after Endoscopic Resection of Early Gastric Cancer

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