title: PPAR-alpha L162V polymorphism in human hepatocellular carcinoma.
abstract: OBJECTIVE
  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 hepatocellular carcinoma and is absent in HCV-related hepatocellular 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.
authors.affiliation: Departments of Gastroenterology and General Surgery, Ankara University, School of Medicine, Ankara.
authors.forename: Elif Sare
authors.initials: ES
authors.lastname: Koytak
authors.forename: Dilşa
authors.initials: D
authors.lastname: Mizrak
authors.forename: Mehmet
authors.initials: M
authors.lastname: Bektaş
authors.forename: Hasibe
authors.initials: H
authors.lastname: Verdi
authors.forename: Ayça
authors.initials: A
authors.lastname: Arslan Ergül
authors.forename: Ramazan
authors.initials: R
authors.lastname: Idilman
authors.forename: Kubilay
authors.initials: K
authors.lastname: Cinar
authors.forename: Cihan
authors.initials: C
authors.lastname: Yurdaydin
authors.forename: Sadik
authors.initials: S
authors.lastname: Ersõz
authors.forename: Kaan
authors.initials: K
authors.lastname: Karayalçin
authors.forename: Ozden
authors.initials: O
authors.lastname: Uzunalimoğlu
authors.forename: Hakan
authors.initials: H
authors.lastname: Bozkaya
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000821:virology*; D016022:Case-Control Studies; D005260:Female; D019694:Hepatitis B, Chronic / Q000150:complications*; D019698:Hepatitis C, Chronic / Q000150:complications*; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics* / Q000821:virology*; D008297:Male; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
chemical_list: D047492:Peroxisome Proliferator-Activated Receptors