VRs, p=0.02), but no significant differences were observed in IL28A and IFNβ expression among patients with different IL28B genotype or treatment response. Conclusion: Induction of IL28B expression by IFN and poly (I:C) stimulation in PBMCs is closely associated with the treatment response to IFN-based therapy. IFNλ4 expression was only detectable in PBMCs derived from patients with ss469415590-dG allele. Impaired IL28B gene induction and expression of IFNλ4 are closely associated with a non-response

to IFN-based therapy in CHC patients. Disclosures: The following people have nothing to disclose: Yasuhiro Asahina, Miyako Murakawa, Sayuri Nitta, INK 128 concentration Yasuhiro Itsui, Mina Nakagawa, Seishin Azuma, Sei Kakinuma, Mamoru Watanabe Background and Aim Aldo-keto reductase family 1, member B10 (AKR1 B10) is an enzyme that converts retinals into retinols, and its up-regulation reduces intracellular retinoic acid, resulting in inhibited cell differentiation. Because AKR1 B1 0 is one of the genes whose expression is increased in human hepatocellular carcinoma (HCC), its involvement in hepatocarcinogenesis is intriguing. We recently analyzed the expression profiles of approximately

41,000 genes in patients with chronic hepatitis C (CHC), and found that AKR1 B1 0 was up-regulated in the livers of patients with CHC who were at DAPT in vivo high risk of developing HCC (Liver Int 2012). The aim of the present study was to elucidate AKR1 B1 0 expression in a large number of patients with CHC and clarify its association

with the risk of HCC development. Methods The study included 338 consecutive patients with CHC who underwent percutaneous liver biopsy. The expression of AKR1B10 in the liver was examined using immunohistochemical analyses and quantified as a percentage of positive staining area using image analysis software. Uni-variate and multivariate Cox proportional hazard analyses were MCE used to estimate the hazard ratios of AKR1 B1 0 expression for HCC development. The cumulative incidences of HCC development were evaluated using Kaplan-Meier plot analysis and the log-rank test. Results The AKR1 B10 expression level in the cohort ranged from 0.0% to 80.1%, and 158 of 338 patients (47%) showed <1.0% AKR1B10 expression. During the median follow-up time of 3.2 years, 28 of the 338 patients developed HCC after liver biopsy. Multivariate Cox proportional hazard analysis demonstrated that high AKR1B10 expression (>6.0%) was an independent risk factor for HCC development (adjusted hazard ratio 3.98, 95% confidence interval 1.43–1 1.09; P = 0.008). The 5-year cumulative incidences of HCC were 19.8% and 2.1% in patients with high and low AKR1 B10 expressions, respectively (P<0.001). In subgroup analyses, the effects of high AKR1 B1 0 expression on the risk of HCC development were significant over strata.