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@ARTICLE{Haselmann:141330,
      author       = {V. Haselmann and C. Gebhardt$^*$ and I. Brechtel and A.
                      Duda and C. Czerwinski and A. Sucker$^*$ and T.
                      Holland-Letz$^*$ and J. Utikal$^*$ and D. Schadendorf$^*$
                      and M. Neumaier},
      title        = {{L}iquid {P}rofiling of {C}irculating {T}umor {DNA} in
                      {P}lasma of {M}elanoma {P}atients for {C}ompanion
                      {D}iagnostics and {M}onitoring of {BRAF} {I}nhibitor
                      {T}herapy.},
      journal      = {Clinical chemistry},
      volume       = {64},
      number       = {5},
      issn         = {1530-8561},
      address      = {Washington, DC},
      publisher    = {American Association for Clinical Chemistry},
      reportid     = {DKFZ-2018-01849},
      pages        = {830 - 842},
      year         = {2018},
      note         = {317},
      abstract     = {The current standard for determining eligibility of
                      patients with metastatic melanoma for BRAF-targeted therapy
                      is tissue-based testing of BRAF mutations. As patients are
                      rarely rebiopsied, detection in blood might be advantageous
                      by enabling a comprehensive assessment of tumor mutational
                      status in real time and thereby representing a noninvasive
                      biomarker for monitoring BRAF therapy.In all, 634 stage I to
                      IV melanoma patients were enrolled at 2 centers, and 1406
                      plasma samples were prospectively collected. Patients were
                      assigned to 3 separate study cohorts: study 1 for assessment
                      of circulating tumor DNA (ctDNA) as part of companion
                      diagnostics, study 2 for assessment of ctDNA for patients
                      with low tumor burden and for follow-up, and study 3 for
                      monitoring of resistance to BRAF inhibitor (BRAFi) or
                      mitogen-activated protein kinase inhibitor therapy.Overall,
                      a high degree of concordance between plasma and tissue
                      testing results was observed at $90.9\%$ (study 1) and
                      $90.1\%$ (study 2), respectively. Interestingly, discrepant
                      results were in some cases associated with nonresponse to
                      BRAFi (n = 3) or a secondary BRAF-mutant malignancy (n = 5).
                      Importantly, ctDNA results correlated with the clinical
                      course of disease in $95.7\%$ and with response to
                      treatment. Significantly, the detection of BRAF mutant ctDNA
                      preceded relapse assessed by Response Evaluation Criteria in
                      Solid Tumors, and was more specific than serum S100 and
                      lactate dehydrogenase.Blood-based testing compares favorably
                      with standard-of-care tissue-based BRAF mutation testing.
                      Importantly, blood-based BRAF testing correlates with the
                      clinical course, even for early-stage patients, and may be
                      used to predict response to treatment, recurrence, and
                      resistance before radioimaging under BRAFi therapy, thereby
                      enabling considerable improvements in patient treatment.},
      cin          = {G300 / C060 / L401},
      ddc          = {610},
      cid          = {I:(DE-He78)G300-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)L401-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29483107},
      doi          = {10.1373/clinchem.2017.281543},
      url          = {https://inrepo02.dkfz.de/record/141330},
}