| Literature DB >> 26890368 |
Dayse Celia Aroucha1,2, Rodrigo Feliciano Carmo3,4, Luydson Richardson Silva Vasconcelos1,5, Raul Emidio Lima6, Taciana Furtado Mendonça4, Lucia Elena Arnez7, Maria do Socorro Mendonça Cavalcanti6, Maria Tereza Cartaxo Muniz6, Marcilio Lins Aroucha8, Erika Rabelo Siqueira1, Luciano Beltrão Pereira1, Patrícia Moura6, Leila Maria Moreira Beltrão Pereira1,2, Maria Rosangela Coêlho9.
Abstract
Hepatitis C virus (HCV) is the major cause of hepatocellular carcinoma (HCC). The risk to develop HCC increases with the severity of liver inflammation and hepatic fibrosis. It is believed that a balance between the releases of pro- and anti-inflammatory cytokines will determine the clinical course of HCV and the risk to develop HCC. The inteleukin-10 (IL-10) and the tumor necrosis factor alpha (TNF-α) play key roles in the Th1 and Th2 balance during the inflammatory response against HCV. The aim of the present study was to investigate the association between polymorphisms in TNF-α -308 G>A (rs1800629), IL-10 -1082 G>A (rs1800896) and -819/-592 (rs1800871/rs1800872) with HCC risk in individuals with HCV. The present study evaluated 388 chronic HCV patients. Polymorphisms were determined by real-time PCR. Diplotypes associated with low IL-10 production and the TNF-α GG genotype were significantly associated with HCC occurrence after multivariate logistic regression analysis (P = 0.027 and P = 0.029, respectively). Additionally, the IL-10 -819 (-592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging (P = 0.044 and P = 0.025, respectively). Patients carrying low production haplotypes of IL-10 and the TNF-α GG genotype have higher risk to develop HCC. J. Med. Virol. 88:1587-1595, 2016.Entities:
Keywords: cytokines; hepatitis c virus; inflammation; interleukin
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Year: 2016 PMID: 26890368 DOI: 10.1002/jmv.24501
Source DB: PubMed Journal: J Med Virol ISSN: 0146-6615 Impact factor: 2.327