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Expression of Smad7 in hepatocellular carcinoma and dysplastic nodules: Resistance mechanism to transforming growth factor-β

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dc.contributor.author박영년-
dc.contributor.author박찬일-
dc.contributor.author최진섭-
dc.date.accessioned2015-07-14T16:44:33Z-
dc.date.available2015-07-14T16:44:33Z-
dc.date.issued2004-
dc.identifier.issn0172-6390-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/111498-
dc.description.abstractBACKGROUND/AIMS: Smad7 is an inhibitory Smad of the transforming growth factor (TGF)-beta signaling pathway. To study resistance mechanisms to antiproliferating effect of TGF-beta in human multistep hepatocarcinogenesis, Smad7, Smad4, TGF-beta1 and TGF-beta receptor II were investigated. METHODOLOGY: Smad7 and Smad4 were evaluated in 15 low-grade dysplastic nodules (DNs), 9 high-grade DNs, 6 early hepatocellular carcinomas (eHCCs) and 41 advanced HCCs by immunohistochemistry and in 37 HCCs and corresponding non-HCCs with fresh tissue, the mRNAs of TGF-beta1 and TGF-beta receptor II were analyzed by RT-PCR. RESULTS: Smad7 immunoreactivity in tumor cells was found in 25 (61%) advanced HCCs, in contrast to none of DNs and eHCCs. Smad7 expression was significantly higher in advanced HCCs with increased TGF-beta1 or no decrease of TGF-beta receptor II compared to those of corresponding non-HCCs (p=0.044, p=0.027). Smad4 expression in stellate cells was present in 28 (68%) advanced HCCs, which was higher in smaller sized and better differentiated HCCs. CONCLUSIONS: Smad7, expressed in tumor cells, is considered to be one of resistance mechanisms to increased TGF-beta1 in late stage hepatocarcinogenesis, especially in advanced HCCs without reduced TGF-beta receptor II. Smad4, in stellate cells of HCCs, might be involved in the host resistance to hepatocarcinogenesis.-
dc.description.statementOfResponsibilityopen-
dc.format.extent396~400-
dc.relation.isPartOfHEPATO-GASTROENTEROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHCarcinoma, Hepatocellular/metabolism*-
dc.subject.MESHDNA-Binding Proteins/metabolism*-
dc.subject.MESHDisease Progression-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHLiver Cirrhosis/metabolism-
dc.subject.MESHLiver Neoplasms/metabolism*-
dc.subject.MESHLiver Neoplasms/physiopathology-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHReceptors, Transforming Growth Factor beta/physiology-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHSignal Transduction-
dc.subject.MESHSmad4 Protein-
dc.subject.MESHSmad7 Protein-
dc.subject.MESHTrans-Activators/metabolism*-
dc.subject.MESHTransforming Growth Factor beta/physiology*-
dc.titleExpression of Smad7 in hepatocellular carcinoma and dysplastic nodules: Resistance mechanism to transforming growth factor-β-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Surgery (외과학)-
dc.contributor.googleauthorYoung Nyun Park-
dc.contributor.googleauthorKwang Jo Chae-
dc.contributor.googleauthorChanil Park-
dc.contributor.googleauthorKyeong Sook Choi-
dc.contributor.googleauthorJinsub Choi-
dc.contributor.googleauthorBong-Kyeong Oh-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.relation.journalcodeJ00984-
dc.identifier.pmid15086168-
dc.identifier.urlhttp://www.hepatogastroenterology.org/index.php/withdrawals/item/4365-expression-of-smad7-in-hepatocellular-carcinoma-and-dysplastic-nodules-resistance-mechanism-to-transforming-growth-factor-%25CE%25B2-
dc.contributor.alternativeNamePark, Young Nyun-
dc.contributor.alternativeNamePark, Chan Il-
dc.contributor.alternativeNameChoi, Jin Sub-
dc.rights.accessRightsnot free-
dc.citation.volume51-
dc.citation.number56-
dc.citation.startPage396-
dc.citation.endPage400-
dc.identifier.bibliographicCitationHEPATO-GASTROENTEROLOGY, Vol.51(56) : 396-400, 2004-
dc.identifier.rimsid34877-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers

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