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Aldo-keto reductase family 1 member B10 is associated with hepatitis B virus-related hepatocellular carcinoma risk.

  • Mori, Masashi1, 2, 3
  • Genda, Takuya1
  • Ichida, Takafumi4
  • Murata, Ayato1
  • Kamei, Masato1
  • Tsuzura, Hironori1
  • Sato, Shunsuke1
  • Narita, Yutaka1
  • Kanemitsu, Yoshio1
  • Ishikawa, Sachiko1
  • Kikuchi, Tetsu1
  • Shimada, Yuji1
  • Hirano, Katsuharu4
  • Iijima, Katsuyori1
  • Sugimoto, Ken2
  • Wada, Ryo5
  • Nagahara, Akihito1
  • Watanabe, Sumio6
  • 1 Department of Gastroenterology and Hepatology, Juntendo University Shizuoka Hospital, Shizuoka, Japan. , (Japan)
  • 2 First Department of Medicine, Hamamatsu University School of Medicine, Shizuoka, Japan. , (Japan)
  • 3 Department of Internal Medicine, Fujinomiya City General Hospital, Shizuoka, Japan. , (Japan)
  • 4 Department of Hepatology, East Shonan General Hospital, Kanagawa, Japan. , (Japan)
  • 5 Department of Pathology, Juntendo University Shizuoka Hospital, Shizuoka, Japan. , (Japan)
  • 6 Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan. , (Japan)
Published Article
Hepatology research : the official journal of the Japan Society of Hepatology
Publication Date
Mar 01, 2017
DOI: 10.1111/hepr.12725
PMID: 27084455


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. 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. 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. 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. © 2016 The Japan Society of Hepatology.

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