% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Breitkreutz:132788,
      author       = {I. Breitkreutz$^*$ and K. Podar$^*$ and V. Figueroa-Vazquez
                      and S. Wilhelm and P. J. Hayden and K. C. Anderson$^*$ and
                      M.-S. Raab$^*$},
      title        = {{T}he orally available multikinase inhibitor regorafenib
                      ({BAY} 73-4506) in multiple myeloma.},
      journal      = {Annals of hematology},
      volume       = {97},
      number       = {5},
      issn         = {0939-5555},
      address      = {Berlin},
      publisher    = {Springer61936},
      reportid     = {DKFZ-2018-00432},
      pages        = {839-849},
      year         = {2018},
      abstract     = {A promising approach to the treatment of multiple myeloma
                      (MM) involves agents that target not only the myeloma cells
                      directly, but also the tumor microenvironment which promotes
                      tumor cell growth, angiogenesis, and MM bone disease. Here
                      we investigate the orally available multikinase inhibitor,
                      regorafenib (BAY 73-4506), for its therapeutic efficacy in
                      MM. Regorafenib is a potent inhibitor of angiogenic (VEGFR
                      1-3, PDGFR-b) as well as oncogenic (c-KIT, RET, FGFR, Raf)
                      kinases. We show that regorafenib induces apoptosis in all
                      MM cell lines at below clinically achievable concentrations.
                      Regorafenib overcomes the growth advantage conferred by a
                      stroma cell MM and an endothelial cell MM, co-culture
                      systems, and abrogates growth factor-stimulated MEK, ERK,
                      and AKT phosphorylation at nanomolar to micromolar
                      concentrations. Moreover, it inhibits endothelial cell
                      growth and tubule formation, abrogates both VEGF secretion
                      and VEGF-induced MM cell migration, inhibits
                      osteoclastogenesis, and shows synergistic cytotoxicity with
                      dexamethasone, the immunomodulatory drug pomalidomide, and
                      the p110δ inhibitor idelalisib. Most importantly,
                      regorafenib significantly delays tumor growth in a xenograft
                      mouse model of human MM. These results provide the rationale
                      for further clinical evaluation of regorafenib, alone and in
                      combination, in the treatment of MM.},
      keywords     = {Phenylurea Compounds (NLM Chemicals) / Protein Kinase
                      Inhibitors (NLM Chemicals) / Pyridines (NLM Chemicals) /
                      regorafenib (NLM Chemicals)},
      cin          = {G170},
      ddc          = {610},
      cid          = {I:(DE-He78)G170-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29359239},
      doi          = {10.1007/s00277-018-3237-5},
      url          = {https://inrepo02.dkfz.de/record/132788},
}