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Virus–host interactions in HBV-related hepatocellular carcinoma: more to be revealed?
  1. Wanlu Cao,
  2. Maikel P Peppelenbosch,
  3. Qiuwei Pan
  1. Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center and Postgraduate School Molecular Medicine, Rotterdam, The Netherlands
  1. Correspondence to Dr Qiuwei Pan, Department of Gastroenterology and Hepatology, Erasmus MC, room Na-617, 'sGravendijkwal 230, Rotterdam NL-3015 CE, The Netherlands; q.pan{at}

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We read with interest the paper by Amaddeo et al 1 describing a comprehensive and integrative study to understand the molecular characteristics of HBV-related hepatocellular carcinoma (HCC). Chronic HBV infection is one of the most common causes of HCC. Although integration of viral gene into host genome has been implicated as an important oncogenic mechanism, a series of studies have reported that both direct and indirect hepatocarcinogenic actions of HBV infection exist. Amaddeo et al 1 found a frequent inactivation of p53 and overexpression of stem cell-related genes in HBV-infected HCC tumours. Most importantly, TP53 mutations were shown to be associated with poor prognosis exclusively in HBV-related patients. This is probably an indirect oncogenic mechanism resulting from HBV infection.

In parallel, in a very recent Cancer Cell paper, …

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  • Contributors WC, MPP, QP discussed and wrote the letter.

  • Funding The authors thank the Netherlands Organization for Scientific Research (NWO/ZonMw) for a VENI grant (No. 916-13-032), the Dutch Digestive Foundation (MLDS) for a career development grant (No. CDG 1304), and the Daniel den Hoed Foundation for a Centennial Award grant (to Q. Pan).

  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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