PMID- 22200181 OWN - NLM STAT- MEDLINE DCOM- 20130221 LR - 20211021 IS - 1000-467X (Print) IS - 1944-446X (Electronic) IS - 1944-446X (Linking) VI - 31 IP - 1 DP - 2012 Jan TI - Tumor necrosis factor-alpha -308G/A polymorphism and risk of hepatocellular carcinoma in hepatitis C virus-infected patients. PG - 29-35 LID - 10.5732/cjc.011.10258 [doi] AB - Tumor necrosis factor-alpha (TNF-alpha) is an important cytokine in generating an immune response against infection with hepatitis C virus (HCV). The functions of TNF-alpha may be altered by single-nucleotide polymorphisms (SNPs) in its gene structure. We hypothesized that SNPs in TNF-alpha may be important in determining the outcome of an HCV infection. To test this hypothesis, we investigated the role of the polymorphism -308G/A, which is located in the promoter region of the TNF-alpha gene, in the progression of HCV infection in Egyptian patients using a quantitative real-time polymerase chain reaction (qRT-PCR). The distribution of this polymorphism and its impact on the serum level of TNF-alpha was compared between 90 HCV-infected patients [45 with HCV-induced cirrhosis and 45 with HCV-related hepatocellular carcinoma (HCC)] and 45 healthy Egyptian volunteers without any history of liver disease. Our results showed that at the TNF-alpha -308 position, the G/G allele was most common (78.5%) in the study population, with the G/A and A/A alleles occurring less frequently (13.3% and 8.1%, respectively). Frequencies of G/G, G/A, and A/A genotypes were 87%, 7%, and 6% in patients with liver cirrhosis and were 94%, 4%, and 2% in patients with HCC, respectively. Serum levels of TNF-alpha were significantly higher in HCV-infected patients than in healthy controls, indicating that the TNF-alpha -308 polymorphism does not influence the production of TNF-alpha. The serum level of TNF-alpha was positively correlated with HCV infection. Taken together, these findings suggest that the TNF-alpha -308 polymorphism may not be a host genetic factor associated with the severity of HCV infection, but may be an independent risk factor for HCC. FAU - Talaat, Roba M AU - Talaat RM AD - Molecular Biology Department, Menofia University, Sadat, Egypt. Robamtalaat@yahoo.com FAU - Esmail, Ahmed A AU - Esmail AA FAU - Elwakil, Reda AU - Elwakil R FAU - Gurgis, Adel A AU - Gurgis AA FAU - Nasr, Mahmoud I AU - Nasr MI LA - eng PT - Journal Article DEP - 20111223 PL - England TA - Chin J Cancer JT - Chinese journal of cancer JID - 101498232 RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Adult MH - Aged MH - Alleles MH - Carcinoma, Hepatocellular/blood/*genetics/virology MH - Female MH - Gene Frequency MH - Genetic Predisposition to Disease MH - Genotype MH - Hepatitis C, Chronic/blood/*genetics MH - Humans MH - Liver Cirrhosis/blood/genetics MH - Liver Neoplasms/blood/*genetics/virology MH - Male MH - Middle Aged MH - *Polymorphism, Single Nucleotide MH - Real-Time Polymerase Chain Reaction MH - Risk Factors MH - Tumor Necrosis Factor-alpha/blood/*genetics PMC - PMC3777466 EDAT- 2011/12/28 06:00 MHDA- 2013/02/22 06:00 PMCR- 2012/01/01 CRDT- 2011/12/28 06:00 PHST- 2011/12/28 06:00 [entrez] PHST- 2011/12/28 06:00 [pubmed] PHST- 2013/02/22 06:00 [medline] PHST- 2012/01/01 00:00 [pmc-release] AID - cjc.011.10258 [pii] AID - cjc-31-01-029 [pii] AID - 10.5732/cjc.011.10258 [doi] PST - ppublish SO - Chin J Cancer. 2012 Jan;31(1):29-35. doi: 10.5732/cjc.011.10258. Epub 2011 Dec 23.