PPAR-alpha L162V polymorphism in human hepatocellular carcinoma

dc.citation.epage249en_US
dc.citation.issueNumber4en_US
dc.citation.spage245en_US
dc.citation.volumeNumber19en_US
dc.contributor.authorKoytak, E. S.en_US
dc.contributor.authorMızrak, D.en_US
dc.contributor.authorBektaş, M.en_US
dc.contributor.authorVerdi, H.en_US
dc.contributor.authorArslan-Ergül, Ayçaen_US
dc.contributor.authorİdilman, R.en_US
dc.contributor.authorÇınar, K.en_US
dc.contributor.authorYurdaydın, C.en_US
dc.contributor.authorErsöz, S.en_US
dc.contributor.authorKarayalçın, K.en_US
dc.contributor.authorUzunalimoğlu, Ö.en_US
dc.contributor.authorBozkaya, H.en_US
dc.contributor.bilkentauthorArslan-Ergül, Ayça
dc.date.accessioned2016-02-08T11:36:44Zen_US
dc.date.available2016-02-08T11:36:44Zen_US
dc.date.issued2008en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractBackground/aims: Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma. Methods: 90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP. Results: hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease. Conclusions: Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced epatocellular carcinoma and is absent in HCV-related epatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression.en_US
dc.identifier.issn1300-4948en_US
dc.identifier.urihttp://hdl.handle.net/11693/26817en_US
dc.language.isoEnglishen_US
dc.publisherTurkish Society of Gastroenterologyen_US
dc.source.titleTurkish Journal of Gastroenterologyen_US
dc.subjectHepatitis B virusen_US
dc.subjectHepatitis C virusen_US
dc.subjectHepatocellular carcinomaen_US
dc.subjectL162Ven_US
dc.subjectPolymorphismen_US
dc.subjectPPARαen_US
dc.subjectCancer diagnosisen_US
dc.subjectCancer stagingen_US
dc.subjectDNA polymorphismen_US
dc.subjectHepatitis delta virusen_US
dc.subjectLiver cell carcinomaen_US
dc.subjectLiver cirrhosisen_US
dc.subjectMajor clinical studyen_US
dc.subjectPathogenesisen_US
dc.subjectPolymerase chain reactionen_US
dc.subjectRestriction fragment length polymorphismen_US
dc.subjectLiver neoplasmsen_US
dc.titlePPAR-alpha L162V polymorphism in human hepatocellular carcinomaen_US
dc.typeConference Paperen_US
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