Title of article :
Cytokine gene polymorphisms in Japanese patients with hepatitis B virus infection—association between TGF-β1 polymorphisms and hepatocellular carcinoma
Author/Authors :
Kiyoshi Migita، نويسنده , , Seiji Miyazoe، نويسنده , , Yumi Maeda، نويسنده , , Manabu Daikoku، نويسنده , , Seigo Abiru، نويسنده , , Tshihito Ueki، نويسنده , , Koji Yano، نويسنده , , Shinya Nagaoka، نويسنده , , Takehiro Matsumoto، نويسنده , , Kazuhiko Nakao، نويسنده , , Keisuke Hamasaki، نويسنده , , Hiroshi Yatsuhashi، نويسنده , , Hiromi Ishibashi، نويسنده , , Katsumi Eguchi، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2005
Pages :
6
From page :
505
To page :
510
Abstract :
Background/Aims In this study, we determined the frequencies of the genotypes associated with the polymorphism of the cytokines genes, and investigated their association with the risk of hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) carriers. Methods Genetic polymorphism in the cytokines TNF-α, IFN-γ, TGF-β1, IL-6, and IL-10 were studied in 236 Japanese patients with HBV infection. The genetic polymorphisms of these cytokines were analyzed by polymerase chain reaction-sequence-specific primer (SSP). Results There was no statistically significant difference in the genetic polymorphisms of TNF-α, IFN-γ, and IL-10 genes between HBV carriers with HCC and those without HCC. However, the TGF-β1+29 (codon 10) C/C genotype was lower in HBV carriers with HCC than in those without HCC (HCC 14.6% vs non-HCC 31.9%). The association of HCC was significantly lower in HBV carriers with C/C genotype than in those with T/C or T/T genotype in position +29 of the TGF-β1 gene. Conclusions Our findings suggest that the genetic polymorphism in codon 10 of the TGF-β1 gene may play a role in HCC development in patients with chronic HBV infection.
Keywords :
cytokines , Transforming growth factor-b1 , polymorphism , hepatitis B virus , Hepatocellular carcinoma
Journal title :
Journal of Hepatology
Serial Year :
2005
Journal title :
Journal of Hepatology
Record number :
586392
Link To Document :
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