Smad2 and Smad4 gene mutations in hepatocellular carcinoma
dc.citation.epage | 4883 | en_US |
dc.citation.issueNumber | 34 | en_US |
dc.citation.spage | 4879 | en_US |
dc.citation.volumeNumber | 18 | en_US |
dc.contributor.author | Yakicier, M. C. | en_US |
dc.contributor.author | Irmak, M. B. | en_US |
dc.contributor.author | Romano, A. | en_US |
dc.contributor.author | Kew, M. | en_US |
dc.contributor.author | Ozturk, M. | en_US |
dc.date.accessioned | 2016-02-08T10:41:06Z | |
dc.date.available | 2016-02-08T10:41:06Z | |
dc.date.issued | 1999 | en_US |
dc.department | Department of Molecular Biology and Genetics | en_US |
dc.description.abstract | TGF-β is a negative regulator of liver growth. Smad family of genes, as mediators of TGF-β pathway, are candidate tumor suppressor genes in hepatocellular carcinoma (HCC). We studied 35 HCC and non-tumour liver tissues for possible mutations in Smad2 and Smad4 genes. Three tumours displayed somatic mutations; two in Smad4 (Asp332Gly and Cys401Arg) and one in Smad2 (Gln407Arg) genes. All three mutations were A:T → G:C transitions suspected to result from oxidative stress as observed in mitochondrial DNA. These observation demonstrate that TGF-β pathway is altered in hepatocellular carcinoma. | en_US |
dc.identifier.doi | 10.1038/sj.onc.1202866 | en_US |
dc.identifier.issn | 0950-9232 | |
dc.identifier.uri | http://hdl.handle.net/11693/25217 | |
dc.language.iso | English | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1038/sj.onc.1202866 | en_US |
dc.source.title | Oncogene | en_US |
dc.subject | Hepatocellular carcinoma | en_US |
dc.subject | Smad2 | en_US |
dc.subject | Smad4 | en_US |
dc.subject | Somatic mutation | en_US |
dc.subject | TGFβ | en_US |
dc.subject | Tumor suppressor genes | en_US |
dc.subject | Mitochondrial DNA | en_US |
dc.title | Smad2 and Smad4 gene mutations in hepatocellular carcinoma | en_US |
dc.type | Article | en_US |
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