pubmed-article:19018769 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0105770 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C1704242 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0387583 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0596263 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C1419067 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:19018769 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:19018769 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:19018769 | pubmed:dateCreated | 2008-12-16 | lld:pubmed |
pubmed-article:19018769 | 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. | lld:pubmed |
pubmed-article:19018769 | pubmed:language | eng | lld:pubmed |
pubmed-article:19018769 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19018769 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19018769 | pubmed:month | Dec | lld:pubmed |
pubmed-article:19018769 | pubmed:issn | 1349-7006 | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:SakaiHirokiH | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:TsukamotoTets... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:YamamotoMasam... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:HirataAkihiro... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:YanaiTokumaT | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:MasegiToshiak... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:TatematsuMasa... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:OshimaMasanob... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:TakasuShinjiS | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:BanHisayoH | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:ToyodaTakeshi... | lld:pubmed |
pubmed-article:19018769 | pubmed:author | pubmed-author:CaoXue-YuanXY | lld:pubmed |
pubmed-article:19018769 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19018769 | pubmed:volume | 99 | lld:pubmed |
pubmed-article:19018769 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19018769 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19018769 | pubmed:pagination | 2356-64 | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:meshHeading | pubmed-meshheading:19018769... | lld:pubmed |
pubmed-article:19018769 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:19018769 | 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. | lld:pubmed |
pubmed-article:19018769 | pubmed:affiliation | Division of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. | lld:pubmed |
pubmed-article:19018769 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19018769 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:19225 | entrezgene:pubmed | pubmed-article:19018769 | lld:entrezgene |
entrez-gene:64292 | entrezgene:pubmed | pubmed-article:19018769 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19018769 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19018769 | lld:entrezgene |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19018769 | lld:pubmed |