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@ARTICLE{Gebhardt:126575,
      author       = {C. Gebhardt$^*$ and A. Sevko$^*$ and H. Jiang$^*$ and R.
                      Lichtenberger$^*$ and M. Reith$^*$ and K. Tarnanidis$^*$ and
                      T. Holland-Letz$^*$ and L. Umansky$^*$ and P. Beckhove$^*$
                      and A. Sucker and D. Schadendorf and J. Utikal$^*$ and V.
                      Umansky$^*$},
      title        = {{M}yeloid {C}ells and {R}elated {C}hronic {I}nflammatory
                      {F}actors as {N}ovel {P}redictive {M}arkers in {M}elanoma
                      {T}reatment with {I}pilimumab.},
      journal      = {Clinical cancer research},
      volume       = {21},
      number       = {24},
      issn         = {1557-3265},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-02603},
      pages        = {5453 - 5459},
      year         = {2015},
      abstract     = {Immunotherapy with ipilimumab improves the survival of
                      patients with metastatic melanoma. Because only around
                      $20\%$ of patients experience long-term benefit, reliable
                      markers are needed to predict a clinical response.
                      Therefore, we sought to determine if some myeloid cells and
                      related inflammatory mediators could serve as predictive
                      factors for the patients' response to ipilimumab.We
                      performed an analysis of myeloid cells in the peripheral
                      blood of 59 stage IV melanoma patients before the treatment
                      and at different time points upon the therapy using a
                      clinical laboratory analysis and multicolor flow cytometry.
                      In addition, the production of related inflammatory factors
                      was evaluated by ELISA or Bio-Plex assays.An early increase
                      in eosinophil count during the treatment with ipilimumab was
                      associated with an improved clinical response. In contrast,
                      elevated amounts of monocytic myeloid-derived suppressor
                      cells (moMDSC), neutrophils, and monocytes were found in
                      nonresponders (n = 36) as compared with basal levels and
                      with responding patients (n = 23). Moreover, in
                      nonresponders, moMDSCs produced significantly more nitric
                      oxide, and granulocytic MDSCs expressed higher levels of
                      PD-L1 than these parameters at baseline and in responders,
                      suggesting their enhanced immunosuppressive capacity. Upon
                      the first ipilimumab infusion, nonresponders displayed
                      elevated serum concentrations of S100A8/A9 and HMGB1 that
                      attract and activate MDSCs.These findings highlight
                      additional mechanisms of ipilimumab effects and suggest
                      levels of eosinophils, MDSCs, as well as related
                      inflammatory factors S100A8/A9 and HMGB1 as novel complex
                      predictive markers for patients who may benefit from the
                      ipilimumab therapy. Clin Cancer Res; 21(24); 5453-9. ©2015
                      AACR.},
      keywords     = {Antibodies, Monoclonal (NLM Chemicals) / Antineoplastic
                      Agents (NLM Chemicals) / Biomarkers (NLM Chemicals) /
                      Inflammation Mediators (NLM Chemicals) / ipilimumab (NLM
                      Chemicals)},
      cin          = {C060 / G300 / D015 / L401},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331 / I:(DE-He78)G300-20160331 /
                      I:(DE-He78)D015-20160331 / 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:26289067},
      doi          = {10.1158/1078-0432.CCR-15-0676},
      url          = {https://inrepo02.dkfz.de/record/126575},
}