PPAR-alpha L162V polymorphism in human hepatocellular carcinoma
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
2008Source 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 PaperItem Usage Stats
105
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30
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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 virusHepatitis 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