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@ARTICLE{Bramante:126175,
      author       = {S. Bramante and J. K. Kaufmann$^*$ and V. Veckman and I.
                      Liikanen and D. Nettelbeck$^*$ and O. Hemminki and L.
                      Vassilev and V. Cerullo and M. Oksanen and R. Heiskanen and
                      T. Joensuu and A. Kanerva and S. Pesonen and S. Matikainen
                      and M. Vähä-Koskela and A. Koski and A. Hemminki},
      title        = {{T}reatment of melanoma with a serotype 5/3 chimeric
                      oncolytic adenovirus coding for {GM}-{CSF}: {R}esults in
                      vitro, in rodents and in humans.},
      journal      = {International journal of cancer},
      volume       = {137},
      number       = {7},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2017-02290},
      pages        = {1775 - 1783},
      year         = {2015},
      abstract     = {Metastatic melanoma is refractory to irradiation and
                      chemotherapy, but amenable to immunological approaches such
                      as immune-checkpoint-inhibiting antibodies or adoptive cell
                      therapies. Oncolytic virus replication is an immunogenic
                      phenomenon, and viruses can be armed with immunostimulatory
                      molecules. Therefore, oncolytic immuno-virotherapy of
                      malignant melanoma is an appealing approach, which was
                      recently validated by a positive phase 3 trial. We
                      investigated the potency of oncolytic adenovirus
                      Ad5/3-D24-GMCSF on a panel of melanoma cell lines and animal
                      models, and summarized the melanoma-specific human data from
                      the Advanced Therapy Access Program (ATAP). The virus
                      effectively eradicated human melanoma cells in vitro and
                      subcutaneous SK-MEL-28 melanoma xenografts in nude mice when
                      combined with low-dose cyclophosphamide. Furthermore,
                      virally-expressed granulocyte-macrophage colony-stimulating
                      factor (GM-CSF) stimulated the differentiation of human
                      monocytes into macrophages. In contrast to human cells, RPMI
                      1846 hamster melanoma cells exhibited no response to
                      oncolytic viruses and the chimeric 5/3 fiber failed to
                      increase the efficacy of transduction, suggesting limited
                      utility of the hamster model in the context of viruses with
                      this capsid. In ATAP, treatments appeared safe and
                      well-tolerated. Four out of nine melanoma patients treated
                      were evaluable for possible therapy benefit with modified
                      RECIST criteria: one patient had minor response, two had
                      stable disease, and one had progressive disease. Two
                      patients were alive at 559 and 2,149 days after treatment.
                      Ad5/3-D24-GMCSF showed promising efficacy in preclinical
                      studies and possible antitumor activity in melanoma patients
                      refractory to other forms of therapy. This data supports
                      continuing the clinical development of oncolytic
                      adenoviruses for treatment of malignant melanoma.},
      keywords     = {Granulocyte-Macrophage Colony-Stimulating Factor (NLM
                      Chemicals) / Cyclophosphamide (NLM Chemicals)},
      cin          = {F110},
      ddc          = {610},
      cid          = {I:(DE-He78)F110-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25821063},
      doi          = {10.1002/ijc.29536},
      url          = {https://inrepo02.dkfz.de/record/126175},
}