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      PPAR-alpha L162V polymorphism in human hepatocellular carcinoma

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      Author
      Koytak, E. S.
      Mızrak, D.
      Bektaş, M.
      Verdi, H.
      Arslan-Ergül, Ayça
      İdilman, R.
      Çınar, K.
      Yurdaydın, C.
      Ersöz, S.
      Karayalçın, K.
      Uzunalimoğlu, Ö.
      Bozkaya, H.
      Date
      2008
      Source Title
      Turkish Journal of Gastroenterology
      Print ISSN
      1300-4948
      Publisher
      Turkish Society of Gastroenterology
      Volume
      19
      Issue
      4
      Pages
      245 - 249
      Language
      English
      Type
      Conference Paper
      Item Usage Stats
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      Abstract
      Background/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.
      Keywords
      Hepatitis B virus
      Hepatitis C virus
      Hepatocellular carcinoma
      L162V
      Polymorphism
      PPARα
      Cancer diagnosis
      Cancer staging
      DNA polymorphism
      Hepatitis delta virus
      Liver cell carcinoma
      Liver cirrhosis
      Major clinical study
      Pathogenesis
      Polymerase chain reaction
      Restriction fragment length polymorphism
      Liver neoplasms
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      http://hdl.handle.net/11693/26817
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