Cited 81 times in
Decreased Helicobacter pylori associated gastric carcinogenesis in mice lacking inducible nitric oxide synthase
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 남기택 | - |
dc.date.accessioned | 2015-07-14T17:30:14Z | - |
dc.date.available | 2015-07-14T17:30:14Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 0017-5749 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/113014 | - |
dc.description.abstract | BACKGROUND AND AIMS: Overproduction of nitric oxide via inducible nitric oxide synthase (iNOS) is suggested to be a significant pathogenic factor in Helicobacter pylori induced gastritis. The purpose of this study was to examine the role of iNOS in H pylori associated gastric carcinogenesis. METHODS: Two types of mice were used in this study: iNOS deficient mice (iNOS-/-) and wild-type littermates. Gastric cancer was generated in mice using a combination treatment comprising N-methyl-N-nitrosourea administration and H pylori infection. Fifty weeks after treatment, tumours in gastric tissues from both types of mice were examined using histopathology, immunohistochemistry, and immunoblotting for iNOS and 3-nitrotyrosine. RESULTS: The overall incidence of gastric cancer at week 50 was significantly lower in iNOS-/- compared with iNOS wild-type mice (p<0.05). When analysed according to tumour pathology, the incidence of gastric adenocarcinoma was significantly lower in iNOS-/- compared with iNOS wild-type mice (p<0.05). Immunostaining for iNOS was clearly observed in adenocarcinoma cells of iNOS wild-type mice, and was characterised by a strong cytoplasmic expression pattern. 3-Nitrotyrosine was expressed mostly in the area of the lamina propria of gastritis and adenoma lesions in iNOS wild-type mice. Immunoblotting analyses showed that iNOS and 3-nitrotyrosine were also expressed in both adenoma and adenocarcinoma tissues from iNOS wild-type mice. iNOS and 3-nitrotyrosine expression was greater in tumour tissues than in non-tumour tissues. CONCLUSIONS: These findings suggest that iNOS contributes to H pylori associated gastric carcinogenesis in mice. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1250~1255 | - |
dc.relation.isPartOf | GUT | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adenocarcinoma/enzymology | - |
dc.subject.MESH | Adenocarcinoma/microbiology | - |
dc.subject.MESH | Adenocarcinoma/pathology | - |
dc.subject.MESH | Adenoma/enzymology | - |
dc.subject.MESH | Adenoma/microbiology | - |
dc.subject.MESH | Adenoma/pathology | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Cell Transformation, Neoplastic/metabolism | - |
dc.subject.MESH | Cell Transformation, Neoplastic/pathology | - |
dc.subject.MESH | Gastric Mucosa/metabolism | - |
dc.subject.MESH | Gastritis/enzymology | - |
dc.subject.MESH | Gastritis/microbiology | - |
dc.subject.MESH | Gastritis/pathology | - |
dc.subject.MESH | Helicobacter Infections/complications* | - |
dc.subject.MESH | Helicobacter pylori*/growth & development | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Mice, Knockout | - |
dc.subject.MESH | Nitric Oxide Synthase/genetics | - |
dc.subject.MESH | Nitric Oxide Synthase/metabolism | - |
dc.subject.MESH | Nitric Oxide Synthase/physiology* | - |
dc.subject.MESH | Nitric Oxide Synthase Type II | - |
dc.subject.MESH | Stomach/microbiology | - |
dc.subject.MESH | Stomach Neoplasms/enzymology | - |
dc.subject.MESH | Stomach Neoplasms/microbiology* | - |
dc.subject.MESH | Stomach Neoplasms/pathology | - |
dc.subject.MESH | Tyrosine/analogs & derivatives* | - |
dc.subject.MESH | Tyrosine/metabolism | - |
dc.title | Decreased Helicobacter pylori associated gastric carcinogenesis in mice lacking inducible nitric oxide synthase | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Life Science (의생명과학부) | - |
dc.contributor.googleauthor | K T Nam | - |
dc.contributor.googleauthor | S-Y Oh | - |
dc.contributor.googleauthor | D-Y Kim | - |
dc.contributor.googleauthor | K-B Hahm | - |
dc.contributor.googleauthor | K-H Yang | - |
dc.contributor.googleauthor | D D Jang | - |
dc.contributor.googleauthor | Y B Kim | - |
dc.contributor.googleauthor | B Ahn | - |
dc.identifier.doi | 10.1136/gut.2003.030684 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01243 | - |
dc.relation.journalcode | J00953 | - |
dc.identifier.eissn | 1468-3288 | - |
dc.identifier.pmid | 15306579 | - |
dc.contributor.alternativeName | Nam, Ki Taek | - |
dc.contributor.affiliatedAuthor | Nam, Ki Taek | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 53 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 1250 | - |
dc.citation.endPage | 1255 | - |
dc.identifier.bibliographicCitation | GUT, Vol.53(9) : 1250-1255, 2004 | - |
dc.identifier.rimsid | 36857 | - |
dc.type.rims | ART | - |
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