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  • Wiley  (3)
  • Genda, Takuya  (3)
  • English  (3)
  • 1
    Online Resource
    Online Resource
    Aldo‐keto reductase family 1 member B10 is associated with hepatitis B virus‐related hepatocellular carcinoma risk
    Wiley ; 2017
    In:  Hepatology Research Vol. 47, No. 3 ( 2017-03)
    Details
    In: Hepatology Research, Wiley, Vol. 47, No. 3 ( 2017-03)
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1386-6346 , 1872-034X
    URL: Issue
    URL: Article
    DOI: 10.1111/hepr.v47.3
    DOI: 10.1111/hepr.12725
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2006439-1
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  • 2
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    Prediction of liver stiffness hepatocellular carcinoma in chronic hepatitis C patients on interferon‐based anti‐viral therapy
    Wiley ; 2014
    In:  Journal of Gastroenterology and Hepatology Vol. 29, No. 1 ( 2014-01), p. 137-143
    Details
    In: Journal of Gastroenterology and Hepatology, Wiley, Vol. 29, No. 1 ( 2014-01), p. 137-143
    Abstract: The purpose of this study was to evaluate the usefulness of liver stiffness measurement ( LSM ) for assessing the risk of hepatocellular carcinoma ( HCC ) in chronic hepatitis C ( CHC ) patients receiving interferon ( IFN ) therapy. Methods One hundred fifty‐one CHC patients who underwent LSM and received IFN therapy were included in the estimation cohort, and 56 were included in the validation study. The cumulative HCC incidences were evaluated using K aplan– M eier plot analysis and the log‐rank test. Multivariate C ox proportional hazard analyses were used to estimate the hazard ratios ( HR s) of variables for HCC . Results In the estimation cohort, 9 of 151 patients developed HCC during the median follow‐up time of 722 days. Multivariate analysis identified three independent risk factors for HCC : LSM (≥ 14.0  kPa , HR 5.58, P  = 0.020), platelet count ( 〈  14.1 × 10 4 / μL , HR 5.59, P  = 0.034), and non‐sustained virological response ( HR 8.28, P  = 0.049). The cumulative incidence of HCC development at 3 years was 59.6%, 8.2%, and 0.0% in patients with all three risk factors, one to two risk factors, and none of these risk factors, respectively. The incidence of HCC was significantly different between these groups ( P   〈  0.001). In the validation cohort, HCC incidence was also significantly different with respect to these risk factors ( P  = 0.037). Conclusion LSM , platelet count, and IFN ‐therapeutic effect could be used to successfully stratify the risk of HCC in patients receiving IFN therapy and demonstrate the usefulness of LSM before IFN therapy for the management of CHC patients.
    Type of Medium: Online Resource
    ISSN: 0815-9319 , 1440-1746
    URL: Issue
    URL: Article
    DOI: 10.1111/jgh.2014.29.issue-1
    DOI: 10.1111/jgh.12401
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2006782-3
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  • 3
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    Online Resource
    Impact of aldo‐keto reductase family 1 member B10 on the risk of hepatitis C virus‐related hepatocellular carcinoma
    Wiley ; 2016
    In:  Journal of Gastroenterology and Hepatology Vol. 31, No. 7 ( 2016-07), p. 1315-1322
    Details
    In: Journal of Gastroenterology and Hepatology, Wiley, Vol. 31, No. 7 ( 2016-07), p. 1315-1322
    Abstract: Aldo‐keto reductase family 1 member B10 (AKR1B10), a cancer‐related oxidoreductase, was recently reported to be upregulated in some chronic liver diseases. However, its relevance in hepatocellular carcinoma (HCC) development is not fully assessed, especially in patients with chronic hepatitis C virus (HCV) infection. Methods Aldo‐keto reductase family 1 member B10 expression in the liver of 550 patients with chronic HCV infection was immunohistochemically assessed and quantified. A multivariate Cox model was used to estimate the hazard ratios (HRs) of AKR1B10 expression for HCC development, and the cumulative incidence of HCC was evaluated using the Kaplan–Meier method. Results Aldo‐keto reductase family 1 member B10 expression in the patients ranged from 0% to 80%. During the median follow‐up of 3.2 years, 43 of 550 patients developed HCC. Multivariate analysis demonstrated that high AKR1B10 expression (≥6%) was an independent risk factor for HCC (HR, 6.43; 95% confidence interval, 2.90–14.25; P   〈  0.001). The 5‐year cumulative incidences of HCC were 22.8% and 2.2% in patients with high and low AKR1B10 expression, respectively ( P   〈  0.001). In subgroup analyses, the effects of high AKR1B10 expression on HCC development risk were significant over strata. In particular, HRs attributed to high AKR1B10 expression were significant in the subgroups that had been considered at a lower risk of HCC, such as in patients with younger age and mild hepatic fibrosis or those who achieved sustained virological response after interferon therapy. Conclusion Various degrees of AKR1B10 upregulation in the liver were observed in patients with chronic HCV infection, and high AKR1B10 expression could be a novel predictor of HCC.
    Type of Medium: Online Resource
    ISSN: 0815-9319 , 1440-1746
    URL: Issue
    URL: Article
    DOI: 10.1111/jgh.2016.31.issue-7
    DOI: 10.1111/jgh.13295
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2006782-3
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