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@ARTICLE{Cheng:126257,
      author       = {P. Cheng and E. Phillips$^*$ and S.-H. Kim and D. Taylor
                      and T. Hielscher$^*$ and L. Puccio$^*$ and A. B. Hjelmeland
                      and P. Lichter$^*$ and I. Nakano and V. Goidts$^*$},
      title        = {{K}inome-wide sh{RNA} screen identifies the receptor
                      tyrosine kinase {AXL} as a key regulator for mesenchymal
                      glioblastoma stem-like cells.},
      journal      = {Stem cell reports},
      volume       = {4},
      number       = {5},
      issn         = {2213-6711},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-02372},
      pages        = {899 - 913},
      year         = {2015},
      abstract     = {Glioblastoma is a highly lethal cancer for which novel
                      therapeutics are urgently needed. Two distinct subtypes of
                      glioblastoma stem-like cells (GSCs) were recently
                      identified: mesenchymal (MES) and proneural (PN). To
                      identify mechanisms to target the more aggressive MES GSCs,
                      we combined transcriptomic expression analysis and
                      kinome-wide short hairpin RNA screening of MES and PN GSCs.
                      In comparison to PN GSCs, we found significant upregulation
                      and phosphorylation of the receptor tyrosine kinase AXL in
                      MES GSCs. Knockdown of AXL significantly decreased MES GSC
                      self-renewal capacity in vitro and inhibited the growth of
                      glioblastoma patient-derived xenografts. Moreover,
                      inhibition of AXL with shRNA or pharmacologic inhibitors
                      also increased cell death significantly more in MES GSCs.
                      Clinically, AXL expression was elevated in the MES GBM
                      subtype and significantly correlated with poor prognosis in
                      multiple cancers. In conclusion, we identified AXL as a
                      potential molecular target for novel approaches to treat
                      glioblastoma and other solid cancers.},
      keywords     = {Antigens, CD44 (NLM Chemicals) / Proto-Oncogene Proteins
                      (NLM Chemicals) / RNA, Small Interfering (NLM Chemicals) /
                      Receptor Protein-Tyrosine Kinases (NLM Chemicals) / axl
                      receptor tyrosine kinase (NLM Chemicals)},
      cin          = {B060 / C060 / B067},
      ddc          = {610},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)B067-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25921812},
      pmc          = {pmc:PMC4437464},
      doi          = {10.1016/j.stemcr.2015.03.005},
      url          = {https://inrepo02.dkfz.de/record/126257},
}