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@ARTICLE{Koch:841559,
      author       = {Koch, Katharina and Hartmann, Rudolf and Suwala, Abigail K.
                      and Rios, Dayana Herrera and Kahlert, Ulf D. and Maciaczyk,
                      Jaroslaw},
      title        = {{A}bstract 2496: {T}argeting brain tumor stem cells by
                      interfering with choline metabolism: {E}vidence for an
                      {EMT}-choline oncometabolic network},
      journal      = {Cancer research},
      volume       = {77},
      number       = {13},
      issn         = {0008-5472},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {FZJ-2017-08597},
      pages        = {2496},
      year         = {2017},
      abstract     = {Glioblastoma (GBM) is the most lethal primary malignant
                      brain tumor with a median survival of less than two years.
                      High levels of therapy resistance, strong cellular
                      invasiveness and rapid cell growth demand aggressive
                      multimodal therapies involving resection as well as
                      radio-chemotherapy. Recent evidence has pointed to the
                      existence of brain tumor stem cells (BTSCs), a subpopulation
                      of human brain tumors which is thought to be responsible for
                      tumor dissemination, relapse and chemo resistance. BTSCs
                      have been associated with the expression of mesenchymal
                      features as a result of epithelial-mesenchymal transition
                      (EMT). Using high resolution proton nuclear magnetic
                      resonance spectroscopy (1H NMR) we compared the
                      intracellular metabolic composition of GBM cells after
                      induction vs. inhibition of EMT as well as under stem cell
                      or differentiated conditions. We identified that both EMT
                      and enrichment for stemness induces the cholinic phenotype
                      which is characterized by high intracellular levels of
                      phosphocholine and total choline derivatives. Furthermore,
                      interference with choline metabolism by targeting choline
                      kinase alpha (CHKα) reversed EMT in GBM cells as we
                      observed reduced invasiveness, clonogenicity, and expression
                      of EMT associated genes. Taken together, interfering with
                      choline metabolism is a powerful strategy to suppress EMT
                      and thus target BTSCs. Moreover, the newly identified
                      BTSC-oncometabolic network could be used to non-invasively
                      monitor the invasive properties of glioblastomas and the
                      success of anti-BTSC therapy.},
      cin          = {ICS-6},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-6-20110106},
      pnm          = {551 - Functional Macromolecules and Complexes (POF3-551)},
      pid          = {G:(DE-HGF)POF3-551},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000442496705345},
      doi          = {10.1158/1538-7445.AM2017-2496},
      url          = {https://juser.fz-juelich.de/record/841559},
}