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dc.contributor.authorAcun T.en_US
dc.contributor.authorTerzioǧlu-Kara, E.en_US
dc.contributor.authorKonu, O.en_US
dc.contributor.authorOzturk, M.en_US
dc.contributor.authorYakicier, M. C.en_US
dc.date.accessioned2016-02-08T10:00:02Z
dc.date.available2016-02-08T10:00:02Z
dc.date.issued2010en_US
dc.identifier.issn1386-1964
dc.identifier.urihttp://hdl.handle.net/11693/22433
dc.description.abstractLoss of function of the p53 protein, which may occur through a range of molecular events, is critical in hepatocellular carcinoma (HCC) evolution. MDM2, an oncogene, acts as a major regulator of the p53 protein. A polymorphism in the MDM2 promoter, SNP309 (T/G), has been shown to alter protein expression and may thus play a role in carcinogenesis. MDM2 SNP309 is also associated with HCC. However, the role of SNP309 in hepatocarcinogenesis with respect to TP53 mutations is unknown. In this study, we investigated the distribution of the MDM2 SNP309 genotype and somatic TP53 (the p53 tumor suppressor gene) mutations in 99 human HCC samples from Africa, Europe, China and Japan. Samples exhibited striking geographical differences in their distribution of SNP309 genotypes. The frequency and spectrum of p53 mutations also varied geographically; TP53 mutations were frequent in Africa, where the SNP309 T/T genotype predominated but were rare in Europe and Japan, where the SNP309 G allele was present more frequently. TP53 mutations were detected in 18% (4/22) of SNP309 T/G and G/G and 82% (18/22) of SNP309 T/T genotype holders; this difference was statistically highly significant (P-value = 0.0006). Our results indicated that the presence of the SNP309 G allele is inversely associated with the presence of somatic TP53 mutations because they only coincided in 4% of HCC cases. This finding suggests that the SNP309 G allele may functionally replace p53 mutations, and in addition to known etiological factors, may be partly responsible for differential HCC prevalence. © 2009 Elsevier B.V. All rights reserved.en_US
dc.language.isoEnglishen_US
dc.source.titleMutation Research - Fundamental and Molecular Mechanisms of Mutagenesisen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.mrfmmm.2009.11.008en_US
dc.subjectHepatocellular carcinomaen_US
dc.subjectMDM2 SNP309en_US
dc.subjectPolymorphismen_US
dc.subjectTP53en_US
dc.subjectguanineen_US
dc.subjectprotein MDM2en_US
dc.subjectprotein p53en_US
dc.subjectthymineen_US
dc.subjectAfricaen_US
dc.subjectalleleen_US
dc.subjectarticleen_US
dc.subjectChinaen_US
dc.subjectcontrolled studyen_US
dc.subjectEuropeen_US
dc.subjectgene frequencyen_US
dc.subjectgene mutationen_US
dc.subjectgenetic associationen_US
dc.subjectgenetic polymorphismen_US
dc.subjectgenetic variabilityen_US
dc.subjectgenotypeen_US
dc.subjecthumanen_US
dc.subjecthuman cellen_US
dc.subjectJapanen_US
dc.subjectliver carcinogenesisen_US
dc.subjectliver cell carcinomaen_US
dc.subjectmajor clinical studyen_US
dc.subjectmolecular mechanicsen_US
dc.subjectprevalenceen_US
dc.subjectpriority journalen_US
dc.subjectpromoter regionen_US
dc.subjectprotein expressionen_US
dc.subjectrace differenceen_US
dc.subjectsingle nucleotide polymorphismen_US
dc.subjectAllelesen_US
dc.subjectCarcinoma, Hepatocellularen_US
dc.subjectGene Frequencyen_US
dc.subjectGenes, p53en_US
dc.subjectHumansen_US
dc.subjectLiver Neoplasmsen_US
dc.subjectMutationen_US
dc.subjectPolymorphism, Single Nucleotideen_US
dc.subjectProto-Oncogene Proteins c-mdm2en_US
dc.subjectTumor Suppressor Protein p53en_US
dc.titleMdm2 Snp309 G allele displays high frequency and inverse correlation with somatic P53 mutations in hepatocellular carcinomaen_US
dc.typeArticleen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.citation.spage106en_US
dc.citation.epage108en_US
dc.citation.volumeNumber684en_US
dc.citation.issueNumber1-2en_US
dc.identifier.doi10.1016/j.mrfmmm.2009.11.008en_US
dc.publisherElsevieren_US


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