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| Expression of HBx protein in hepatitis B virus-infected intrahepatic cholangiocarcinoma |
| Yan-Ming Zhou, Lu Cao, Bin Li, Xiu-Zhong Zhang and Zheng-Feng Yin |
Shanghai, China
Author Affiliations: Department of Hepato-Biliary-Pancreato-Vascular Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China (Zhou YM and Li B); Department of Molecular Oncology (Cao L and Yin ZF) and Department of Pathology (Zhang XZ), Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, China
Corresponding Author: Zheng-Feng Yin, MD, PhD, Department of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, China (Tel: 86-21-81875351; Fax: 86-21-81862400; Email: yinzfk@yahoo.com.cn) |
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Abstract BACKGROUND: Hepatitis B virus (HBV) is an etiological factor of intrahepatic cholangiocarcinoma (ICC), but the pathogenic mechanisms remain unclear. This study aimed to investigate the expression and possible role of HBx, an HBV-encoded potentially oncogenic protein, in HBV-infected ICC.
METHODS: Tissue samples were obtained from 54 specimens of HBV-infected ICC. Forty-four specimens were of peripheral type and 10 hilar type. Formalin-fixed, paraffin-embedded sections of the specimens were immunohistochemically stained for HBx and p53.
RESULTS: HBx expression was found in 70.4% (38/54) of the specimens, and it was more frequently seen in the peripheral type than in the hilar type (79.5% vs 30.0%, P=0.002). All three well-differentiated ICCs expressed HBx, whereas 76.9% (30/39) moderately-differentiated and 41.7% (5/12) poorly-differentiated ICCs had HBx expression (P=0.033). Patients with HBx expression had a significantly higher prevalence of elevated serum alpha-fetoprotein (P=0.033). p53 protein expression was found in 18 of 54 cases (33.3%), and was not correlated with that of HBx.
CONCLUSIONS: HBx may contribute to the pathogenesis of ICC, particularly the peripheral type. p53 abnormality may not play a significant role in HBx-mediated oncogenicity during ICC carcinogenesis.
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2012, Vol. 11 
