Aldo‐keto reductase family 1 member B10 is associated with hepatitis B virus‐related hepatocellular carcinoma risk. Issue 3 (11th May 2016)

• Record Type: Journal Article
• Authors: Mori, Masashi; Genda, Takuya; Ichida, Takafumi; Murata, Ayato; Kamei, Masato; Tsuzura, Hironori; Sato, Shunsuke; Narita, Yutaka; Kanemitsu, Yoshio; Ishikawa, Sachiko; Kikuchi, Tetsu; Shimada, Yuji; Hirano, Katsuharu; Iijima, Katsuyori; Sugimoto, Ken; Wada, Ryo; Nagahara, Akihito; Watanabe, Sumio
• Is Part Of: Hepatology research. Volume 47:Issue 3(2017)
• Page Start: E85
• Page End: E93
• Publication Date: 2016-05-11
• Subjects: AKR1B10 protein -- carcinoma -- chronic -- hepatitis b -- hepatocellular -- risk factors; Liver -- Diseases -- Periodicals; Liver Diseases -- Periodicals; Foie -- Maladies -- Périodiques; 616.362
• DOI: 10.1111/hepr.12725
• Languages: English
• ISSNs: 1386-6346

Abstract

Abstract : Aim: Recent reports have indicated that aldo‐keto reductase family 1 member B10 (AKR1B10), a cancer‐related oxidoreductase, was upregulated in some chronic liver diseases. However, few studies have reported AKR1B10 expression in chronic hepatitis B virus (HBV)‐infected patients. The aim of the present study was to analyze AKR1B10 expression and its relevance on hepatocellular carcinoma (HCC) development in patients with chronic HBV infection. Methods: Expression of AKR1B10 in the liver of 119 chronic HBV‐infected patients was assessed and quantified immunohistochemically. A multivariate Cox model was used to estimate the hazard ratios of AKR1B10 expression for HCC development. The cumulative incidences of HCC were evaluated using Kaplan–Meier analysis. Results: Expression of AKR1B10 in the study cohort ranged from 0% to 84%. During the median follow‐up time (6.2 years), 13 patients developed HCC. Multivariate analysis revealed that high AKR1B10 expression (≥15%) was an independent risk factor for HCC (hazard ratio, 10.8; 95% confidence interval, 3.0–38.6; P < 0.001). The 5‐year cumulative incidences of HCC were 20.6% and 2.6% in patients with high and low AKR1B10 expression, respectively ( P < 0.001). Patients with high AKR1B10 expression had significantly higher alanine aminotransferase levels during follow‐up than those with low expression, even though antiviral treatment decreased HBV‐DNA levels in both groups. Conclusion: Chronic HBV‐infected patients with high hepatic AKR1B10 expression had an increased risk of HCC development. This suggests that AKR1B10 upregulation might play a role in the early stages of HBV‐related hepatocarcinogenesis.