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@ARTICLE{Chudasama:119837,
      author       = {P. Chudasama$^*$ and M. Renner and M. Straub and S. S.
                      Mughal$^*$ and B. Hutter$^*$ and Z. Kosaloglu-Yalcin$^*$ and
                      R. Schweßinger$^*$ and M. Scheffler and I. Alldinger and S.
                      Schimmack and T. Persigehl and C. Kobe and D. Jäger$^*$ and
                      C. von Kalle$^*$ and P. Schirmacher and M.-K. Beckhaus$^*$
                      and S. Wolf$^*$ and C. Heining and S. Gröschel$^*$ and J.
                      Wolf and B. Brors$^*$ and W. Weichert and H. Glimm$^*$ and
                      C. Scholl$^*$ and G. Mechtersheimer and K. Specht and S.
                      Fröhling$^*$},
      title        = {{T}argeting {F}ibroblast {G}rowth {F}actor {R}eceptor 1 for
                      {T}reatment of {S}oft-{T}issue {S}arcoma.},
      journal      = {Clinical cancer research},
      volume       = {23},
      number       = {4},
      issn         = {1557-3265},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-00432},
      pages        = {962 - 973},
      year         = {2017},
      abstract     = {Purpose: Altered FGFR1 signaling has emerged as a
                      therapeutic target in epithelial malignancies. In contrast,
                      the role of FGFR1 in soft-tissue sarcoma (STS) has not been
                      established. Prompted by the detection and subsequent
                      therapeutic inhibition of amplified FGFR1 in a patient with
                      metastatic leiomyosarcoma, we investigated the oncogenic
                      properties of FGFR1 and its potential as a drug target in
                      patients with STS.Experimental Design: The frequency of
                      FGFR1 amplification and overexpression, as assessed by FISH,
                      microarray-based comparative genomic hybridization and mRNA
                      expression profiling, SNP array profiling, and RNA
                      sequencing, was determined in three patient cohorts. The
                      sensitivity of STS cell lines with or without FGFR1
                      alterations to genetic and pharmacologic FGFR1 inhibition
                      and the signaling pathways engaged by FGFR1 were
                      investigated using viability assays, colony formation
                      assays, and biochemical analysis.Results: Increased FGFR1
                      copy number was detected in 74 of 190 $(38.9\%;$ cohort 1),
                      13 of 79 $(16.5\%;$ cohort 2), and 80 of 254 $(31.5\%;$
                      cohort 3) patients. FGFR1 overexpression occurred in 16 of
                      79 $(20.2\%,$ cohort 2) and 39 of 254 $(15.4\%;$ cohort 3)
                      patients. Targeting of FGFR1 by RNA interference and
                      small-molecule inhibitors (PD173074, AZD4547, BGJ398)
                      revealed that the requirement for FGFR1 signaling in STS
                      cells is dictated by FGFR1 expression levels, and identified
                      the MAPK-ERK1/2 axis as critical FGFR1 effector
                      pathway.Conclusions: These data identify FGFR1 as a driver
                      gene in multiple STS subtypes and support FGFR1 inhibition,
                      guided by patient selection according to the FGFR1
                      expression and monitoring of MAPK-ERK1/2 signaling, as a
                      therapeutic option in this challenging group of diseases.
                      Clin Cancer Res; 23(4); 962-73. ©2016 AACR.},
      cin          = {G100 / G200 / D120 / G010 / W190 / G102 / G240 / L101 /
                      L701},
      ddc          = {610},
      cid          = {I:(DE-He78)G100-20160331 / I:(DE-He78)G200-20160331 /
                      I:(DE-He78)D120-20160331 / I:(DE-He78)G010-20160331 /
                      I:(DE-He78)W190-20160331 / I:(DE-He78)G102-20160331 /
                      I:(DE-He78)G240-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)L701-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27535980},
      doi          = {10.1158/1078-0432.CCR-16-0860},
      url          = {https://inrepo02.dkfz.de/record/119837},
}