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@ARTICLE{Waldt:157728,
      author       = {Waldt, Natalie and Kesseler, Christoph and Fala, Paula and
                      John, Peter and Kirches, Elmar and Angenstein, Frank and
                      Mawrin, Christian},
      title        = {{C}rispr/{C}as-based modeling of {NF}2 loss in meningioma
                      cells.},
      journal      = {Journal of neuroscience methods},
      volume       = {356},
      issn         = {0165-0270},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2021-01185},
      pages        = {109141},
      year         = {2021},
      abstract     = {Alterations of the neurofibromatosis type 2 gene (NF2)
                      occur in more than fifty percent of sporadic meningiomas.
                      Meningiomas develop frequently in the setting of the
                      hereditary tumor syndrome NF2. Investigation of potential
                      drug-based treatment options has been limited by the lack of
                      appropriate in vitro and in vivo models.Using Crispr/Cas
                      gene editing, of the malignant meningioma cell line
                      IOMM-Lee, we generated a pair of cell clones characterized
                      by either stable knockout of NF2 and loss of the protein
                      product merlin or retained merlin protein (transfected
                      control without gRNA).IOMM-Lee cells lacking NF2 showed
                      reduced apoptosis and formed bigger colonies compared to
                      control IOMM-Lee cells. Treatment of non-transfected
                      IOMM-Lee cells with the focal adhesion kinase (FAK)
                      inhibitor GSK2256098 resulted in reduced colony sizes.
                      Orthotopic mouse xenografts showed the formation of
                      convexity tumors typical for meningiomas with NF2-depleted
                      and control cells.No orthotopic meningioma models with
                      genetically-engineered cell pairs are available so far.Our
                      model based on Crispr/Cas-based gene editing provides paired
                      meningioma cells suitable to study functional consequences
                      and therapeutic accessibility of NF2/merlin loss.},
      keywords     = {Animals / Cell Line, Tumor / Clustered Regularly
                      Interspaced Short Palindromic Repeats: genetics / Meningeal
                      Neoplasms: genetics / Meningioma: genetics / Mice /
                      Neurofibromin 2: genetics / Neurofibromin 2: metabolism /
                      Crispr/Cas (Other) / Meningioma (Other) / Neurofibromatosis
                      type 2 (NF2) (Other) / Neurofibromin 2 (NLM Chemicals)},
      cin          = {AG Angenstein},
      ddc          = {610},
      cid          = {I:(DE-2719)1310004},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33753124},
      doi          = {10.1016/j.jneumeth.2021.109141},
      url          = {https://pub.dzne.de/record/157728},
}