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@ARTICLE{Heller:134852,
      author       = {M. Heller and E.-S. Prigge$^*$ and A. Kaczorowski and M.
                      von Knebel Doeberitz$^*$ and M. Hohenfellner and S.
                      Duensing},
      title        = {{APOBEC}3{A} {E}xpression in {P}enile {S}quamous {C}ell
                      {C}arcinoma.},
      journal      = {Pathobiology},
      volume       = {85},
      number       = {3},
      issn         = {1423-0291},
      address      = {Basel},
      publisher    = {Karger},
      reportid     = {DKFZ-2018-00642},
      pages        = {169 - 178},
      year         = {2018},
      abstract     = {APOBECs (apolipoprotein B mRNA-editing catalytic
                      polypeptides) are cytidine deaminases that have been
                      implicated in the host defense against viruses by blocking
                      viral replication. They have also been shown to play a role
                      in genome hypermutation in several human cancers. An APOBEC3
                      hypermutation signature has been discovered in cervical
                      cancer, which is intimately associated with infection by
                      high-risk human papillomaviruses (HPVs). At the same time,
                      HPV genomes themselves are subject to DNA editing by
                      APOBECs. Similar to cervical cancer, a proportion of penile
                      squamous cell carcinomas (SCCs) is etiologically driven by
                      high-risk HPVs, but very little is known about the role of
                      APOBECs in penile SCC development and progression.A series
                      of 34 penile SCCs was analyzed for the expression of
                      APOBEC3A protein by immunohistochemistry. HPV genotyping was
                      carried out using a bead-based multiplex hybridization assay
                      preceded by BSGP5+6+ primer-based amplification.We found a
                      frequent reduction of APOBEC3A protein expression in the
                      invasive parts of the majority of HPV-negative penile SCCs.
                      In contrast, the majority of HPV-positive penile SCCs
                      retained APOBEC3A expression during malignant
                      progression.Our results suggest that APOBEC3A expression is
                      downregulated during progression towards invasiveness in
                      HPV-negative penile SCC, but maintained in HPV-positive
                      penile SCC. How high-risk HPV-infected tumor cells tolerate
                      high APOBEC3A, which appears to exert tumor suppressive
                      functions in HPV-negative penile SCCs, remains to be
                      elucidated.},
      cin          = {G105},
      ddc          = {610},
      cid          = {I:(DE-He78)G105-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29166639},
      doi          = {10.1159/000479007},
      url          = {https://inrepo02.dkfz.de/record/134852},
}