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@ARTICLE{BoscoloRizzo:144580,
      author       = {P. Boscolo-Rizzo and L. Schroeder$^*$ and V. Sacchetto and
                      D. Holzinger$^*$ and M. C. Da Mosto and G. Tirelli and E.
                      Dal Cin and M. Mantovani and A. Menegaldo and A. Del Mistro
                      and S. Romeo and A. P. Dei Tos and M. Niero and S. Rigo and
                      G. Dyckhoff and J. Hess$^*$ and L. Alemany and M. Quer and
                      X. León and J. Polesel and M. Pawlita$^*$ and R.
                      Bertorelle},
      title        = {{A}bsence of disruptive {TP}53 mutations in high-risk human
                      papillomavirus-driven neck squamous cell carcinoma of
                      unknown primary.},
      journal      = {Head $\&$ neck},
      volume       = {41},
      number       = {11},
      issn         = {1097-0347},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {DKFZ-2019-02023},
      pages        = {3833-3841},
      year         = {2019},
      note         = {Head Neck. 2019 Nov;41(11):3833-3841},
      abstract     = {To enforce the evidence for causality between high-risk
                      human papillomavirus (hrHPV) infections and neck squamous
                      cell carcinoma from unknown primary (NSCCUP) and provide
                      biological basis for treatment de-intensification, we
                      searched for TP53 mutations in association with HPV
                      status.TP53 mutations were searched for by amplification of
                      exons 4 to 10.Of the 70 NSCCUP, 27 $(39\%)$ harbored HPV
                      infection. TP53 sequencing resulted in the identification of
                      19 patients harboring single mutations including 16
                      disruptive alterations $(84\%).$ The association of TP53
                      mutations and HPV could be evaluated in 48 NSCCUP including
                      those with disruptive mutation in any exon (n = 16) and
                      those without mutations but with complete sequence of exons
                      4 to 9 (n = 32): no disruptive mutations were found in the
                      17 HPV-driven NSCCUP but in 16 of the 31 non-HPV-driven
                      NSCCUP (P = .0002).In a fraction of cases, NSCCUP is an
                      HPV-driven entity harboring wild-type TP53 gene or
                      nondisruptive TP53 mutations. HPV-driven NSCCUP might
                      benefit from treatment de-intensification.},
      cin          = {F022 / F020 / A102},
      ddc          = {610},
      cid          = {I:(DE-He78)F022-20160331 / I:(DE-He78)F020-20160331 /
                      I:(DE-He78)A102-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31414564},
      doi          = {10.1002/hed.25915},
      url          = {https://inrepo02.dkfz.de/record/144580},
}