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Conditional loss of TGF-beta signalling leads to increased susceptibility to gastrointestinal carcinogenesis in mice.

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dc.contributor.authorHahm, KB-
dc.contributor.authorLee, KM-
dc.contributor.authorKim, YB-
dc.contributor.authorHong, WS-
dc.contributor.authorLee, WH-
dc.contributor.authorHan, SU-
dc.contributor.authorKim, MW-
dc.contributor.authorAhn, BO-
dc.contributor.authorOh, TY-
dc.contributor.authorLee, MH-
dc.contributor.authorGreen, J-
dc.contributor.authorKim, SJ-
dc.date.accessioned2011-07-20-
dc.date.available2011-07-20-
dc.date.issued2002-
dc.identifier.issn0269-2813-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3459-
dc.description.abstractBACKGROUND: Downregulation of TGF-beta receptors is implicated in colon cancer development. Inactivation of either of the two transmembrane serine/threonine kinases, TGF-beta1 types I/II receptors, is now implicated in carcinogenesis, especially gastrointestinal carcinogenesis.
METHODS: We generated transgenic mice, called pS2-dnRII or ITF-dnRII, of which the dominant negative mutant of the TGF-beta type II receptor was expressed under the control of tissue-specific promoters, the pS2 promoter for stomach and ITF for intestine. They were either infected with H.pylori (ATCC 43504 strain, CagA+ and VacA+) or administered with azoxymethane to determine the significance of loss of TGF-beta signalling in gastrointestinal carcinogenesis.
RESULTS: Gastric adenocarcinoma developed in pS2-dnRII mice, whereas only chronic active gastritis was noted in wild-type littermates after 36 weeks of H.pylori infection. Mice lacking in TGF-beta signalling specifically in the stomach showed a significantly higher proliferation cell nuclear antigen-labelling index when infected with H.pylori than wild-type littermates (P < 0.01). Development of colonic aberrant crypt foci was provoked in mice by intraperitoneal injections of azoxymethane, and ITF-dnRII mice showed significantly higher incidences of ACF and colon cancers than wild-type littermates.
CONCLUSIONS: Maintaining normal TGF-beta signalling in the gastrointestinal tract seems to be important either for preventing abnormal mucosal proliferation, or for suppressing or retarding carcinogenesis.
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dc.formatapplication/pdf-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHAzoxymethane-
dc.subject.MESHCarcinogens-
dc.subject.MESHCarcinoma-
dc.subject.MESHColonic Neoplasms-
dc.subject.MESHDisease Susceptibility-
dc.subject.MESHGastritis-
dc.subject.MESHHelicobacter Infections-
dc.subject.MESHHelicobacter pylori-
dc.subject.MESHMice-
dc.subject.MESHMice, Transgenic-
dc.subject.MESHReceptors, Transforming Growth Factor beta-
dc.subject.MESHSignal Transduction-
dc.subject.MESHStomach Neoplasms-
dc.subject.MESHTransforming Growth Factor beta-
dc.titleConditional loss of TGF-beta signalling leads to increased susceptibility to gastrointestinal carcinogenesis in mice.-
dc.typeArticle-
dc.identifier.pmid11966532-
dc.identifier.urlhttps://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0269-2813&date=2002&volume=16&issue=&spage=115-
dc.contributor.affiliatedAuthor함, 기백-
dc.contributor.affiliatedAuthor이, 기명-
dc.type.localJournal Papers-
dc.identifier.doi10.1046/j.1365-2036.16.s2.3.x-
dc.citation.titleAlimentary pharmacology & therapeutics-
dc.citation.volume16-
dc.citation.numbersuppl.2-
dc.citation.date2002-
dc.citation.startPage115-
dc.citation.endPage127-
dc.identifier.bibliographicCitationAlimentary pharmacology & therapeutics, 16(suppl.2). : 115-127, 2002-
dc.identifier.eissn1365-2036-
dc.relation.journalidJ002692813-
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Journal Papers > School of Medicine / Graduate School of Medicine > Gastroenterology
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