Source:http://linkedlifedata.com/resource/pubmed/id/19018769
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2008-12-16
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pubmed:abstractText |
K19-C2mE transgenic (Tg) mice, simultaneously expressing cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) in the gastric mucosa under the cytokeratin 19 gene promoter, were here treated with N-methyl-N-nitrosourea (MNU) and inoculated with Helicobacter pylori (H. pylori) to investigate gastric carcinogenesis. Wild-type (WT) and Tg mice undergoing MNU treatment frequently developed tumors in the pyloric region (100% and 94.7%, respectively); multiplicity in Tg was higher than that in WT (P < 0.05) with H. pylori infection. Larger pyloric tumors were more frequently observed in Tg than in WT (P < 0.05). In addition, Tg developed fundic tumors, where WT did not. No gastric tumors were observed without MNU treatment. Transcripts of TNF-alpha, iNOS, IL-1beta, and CXCL14 were up-regulated with H. pylori infection in both genotypes and were also increased more in Tg than in WT within H. pylori-inoculated animals. Immunohistochemical analysis demonstrated significantly greater beta-catenin accumulation in pyloric tumors, compared with those in the fundus (P < 0.01) with mutations of exon 3; 18.2% and 31.6% in MNU-alone and MNU + H. pylori-treated WT, whereas 21.4% and 62.5% was observed in the Tg, respectively; the latter significantly higher (P < 0.05), suggesting the role of H. pylori in Wnt activation. In conclusion, K19-C2mE mice promoted gastric cancer in both fundic and pyloric regions. Furthermore beta-catenin activation may play the important role of pyloric carcinogenesis especially in H. pylori-infected Tg. Induction of various inflammatory cytokines in addition to overexpression of COX-2/mPGES-1 could be risk factors of gastric carcinogenesis and may serve as a better gastric carcinogenesis model.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Intramolecular Oxidoreductases,
http://linkedlifedata.com/resource/pubmed/chemical/Methylnitrosourea,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin,
http://linkedlifedata.com/resource/pubmed/chemical/prostaglandin-E synthase
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1349-7006
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pubmed:author |
pubmed-author:BanHisayoH,
pubmed-author:CaoXue-YuanXY,
pubmed-author:HirataAkihiroA,
pubmed-author:MasegiToshiakiT,
pubmed-author:OshimaMasanobuM,
pubmed-author:SakaiHirokiH,
pubmed-author:TakasuShinjiS,
pubmed-author:TatematsuMasaeM,
pubmed-author:ToyodaTakeshiT,
pubmed-author:TsukamotoTetsuyaT,
pubmed-author:YamamotoMasamiM,
pubmed-author:YanaiTokumaT
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pubmed:issnType |
Electronic
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pubmed:volume |
99
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2356-64
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pubmed:meshHeading |
pubmed-meshheading:19018769-Animals,
pubmed-meshheading:19018769-Carcinogens,
pubmed-meshheading:19018769-Cell Transformation, Neoplastic,
pubmed-meshheading:19018769-Cyclooxygenase 2,
pubmed-meshheading:19018769-Enzyme Activation,
pubmed-meshheading:19018769-Gastric Mucosa,
pubmed-meshheading:19018769-Helicobacter Infections,
pubmed-meshheading:19018769-Helicobacter pylori,
pubmed-meshheading:19018769-Immunohistochemistry,
pubmed-meshheading:19018769-Intramolecular Oxidoreductases,
pubmed-meshheading:19018769-Methylnitrosourea,
pubmed-meshheading:19018769-Mice,
pubmed-meshheading:19018769-Mice, Transgenic,
pubmed-meshheading:19018769-Microsomes,
pubmed-meshheading:19018769-Random Allocation,
pubmed-meshheading:19018769-Stomach Neoplasms,
pubmed-meshheading:19018769-beta Catenin
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pubmed:year |
2008
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pubmed:articleTitle |
Roles of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression and beta-catenin activation in gastric carcinogenesis in N-methyl-N-nitrosourea-treated K19-C2mE transgenic mice.
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pubmed:affiliation |
Division of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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