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@ARTICLE{Herzer:120385,
      author       = {K. Herzer and G. Gerken and T. Hofmann$^*$},
      title        = {{H}epatitis {C}-associated liver carcinogenesis: role of
                      {PML} nuclear bodies.},
      journal      = {World journal of gastroenterology},
      volume       = {20},
      number       = {35},
      issn         = {1007-9327},
      address      = {Beijing},
      publisher    = {WJG Press},
      reportid     = {DKFZ-2017-00818},
      pages        = {12367 -},
      year         = {2014},
      abstract     = {Successful escape from immune response characterises
                      chronic hepatitis C virus (HCV) infection, which results in
                      persistence of infection in about $80\%$ of the patients.
                      The deleterious consequences are cirrhosis and
                      hepatocellular carcinoma. HCV accounts the most frequent
                      cause for hepatocellular carcinoma (HCC) and liver
                      transplantation (LT) in the western world. The underlying
                      molecular mechanisms how HCV promotes tumor development are
                      largely unknown. There is some in vitro and in vivo evidence
                      that HCV interferes with the tumor suppressor PML and may
                      thereby importantly contribute to the HCV-associated
                      pathogenesis with respect to the development of HCC. The
                      tumor suppressor protein 'promyelocytic leukemia' (PML) has
                      been implicated in the regulation of important cellular
                      processes like differentiation and apoptosis. In cancer
                      biology, PML and its associated nuclear bodies (NBs) have
                      initially attracted intense interest due to its role in the
                      pathogenesis of acute promyelocytic leukemia (APL). More
                      recently, loss of PML has been implicated in human cancers
                      of various histologic origins. Moreover, number and
                      intensity of PML-NBs increase in response to interferons
                      (IFNs) and there is evidence that PML-NBs may represent
                      preferential targets in viral infections. Thus, PML could
                      not only play a role in the mechanisms of the antiviral
                      action of IFNs but may also be involved in a direct
                      oncogenic effect of the HCV on hepatocytes. This review aims
                      to summarise current knowledge about HCV-related liver
                      carcinogenesis and to discuss a potential role of the
                      nuclear body protein PML for this this hard-to-treat
                      cancer.},
      subtyp        = {Review Article},
      keywords     = {Nuclear Proteins (NLM Chemicals) / Promyelocytic Leukemia
                      Protein (NLM Chemicals) / Transcription Factors (NLM
                      Chemicals) / Tumor Suppressor Proteins (NLM Chemicals) / PML
                      protein, human (NLM Chemicals)},
      cin          = {A210},
      ddc          = {610},
      cid          = {I:(DE-He78)A210-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25253937},
      pmc          = {pmc:PMC4168070},
      doi          = {10.3748/wjg.v20.i35.12367},
      url          = {https://inrepo02.dkfz.de/record/120385},
}