ABSTRACT
BACKGROUND/AIMS: To clarify any association between the hOGG1 Ser326Cys polymorphism and susceptibility to hepatocellular carcinoma (HCC). METHODOLOGY: The PubMed, CNKI databases were searched for all available articles. The OR corresponding to the 95% confidence interval (95% CI) was used to assess the association between hOGG1 Ser326Cys polymorphism and susceptibility to HCC. RESULTS: Seven case-control studies, with 1,663 cases and 1,675 controls, were available for this analysis. No association was found between hOGG1 Ser326Cys polymorphism and HCC risk (dominant model: OR=0.695, 95% CI: 0.501-0.964, p=0.029; additive model: OR=0.682, 95% CI: 0.374-1.245, p=0.213; recessive model: OR=1.215, 95% CI: 0.711-2.078, p=0.476). Sensitivity analysis did not perturb the results. CONCLUSIONS: These findings indicated that hOGG1 Ser326Cys polymorphism may not play a role in HCC development. However, larger scale studies are needed for confirmation.
Subject(s)
Carcinoma, Hepatocellular/genetics , DNA Glycosylases/genetics , Genetic Predisposition to Disease , Liver Neoplasms/genetics , Polymorphism, Genetic , Case-Control Studies , Humans , Publication BiasABSTRACT
Avian influenza virus subtype H9N2 has been circulating in multiple terrestrial birds and repeatedly infecting mammals, including swines and humans to pose a significant threat to public health. The cross-species infection of human, replication activity and tissue tropism of avian influenza virus H9N2 was evaluated in this study. The results showed that surgically removed human lung tissue samples were infected ex vivo by avian influenza virus subtype H9N2 (Ck/GX/1875/04, Ck/GX/187/05) and seasonal human influenza virus H3N2 (A/ST/602/05). Examination of nucleoprotein expression replication in the infected human lung tissue samples showed that the replication of avian influenza virus H9N2 and seasonal human influenza virus H3N2 were mainly prevalent in alveolar epithelial cells, respiratory bronchiole epithelial cells and bronchial epithelial cells. Double-immunostaining for viral antigens and cellular markers indicated that avian influenza virus subtype H9N2 replicated in type 2 alveolar epithelial cells. These findings suggest that the H9N2 virus may be better adapted to the human host and replicates efficiently in human lung epithelial cells. Moreover, H9N2 avian influenza virus repeatedly infecting human, may favor gene evolution and the potential emergence of pandemic influenza virus.