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@ARTICLE{Alimova:181116,
      author       = {I. Alimova and A. M. Pierce and P. Harris and A. Donson and
                      D. K. Birks and E. Prince and I. Balakrishnan and N. K.
                      Foreman and M. Kool$^*$ and L. Hoffman and S. Venkataraman
                      and R. Vibhakar},
      title        = {{T}argeting {P}olo-like kinase 1 in {SMARCB}1 deleted
                      atypical teratoid rhabdoid tumor.},
      journal      = {OncoTarget},
      volume       = {8},
      number       = {57},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2022-01785},
      pages        = {97290 - 97303},
      year         = {2017},
      abstract     = {Atypical teratoid rhabdoid tumor (ATRT) is an aggressive
                      and malignant pediatric brain tumor. Polo-like kinase 1
                      (PLK1) is highly expressed in many cancers and essential for
                      mitosis. Overexpression of PLK1 promotes chromosome
                      instability and aneuploidy by overriding the G2-M DNA damage
                      and spindle checkpoints. Recent studies suggest that
                      targeting PLK1 by small molecule inhibitors is a promising
                      approach to tumor therapy. We investigated the effect of
                      PLK1 inhibition in ATRT. Gene expression analysis showed
                      that PLK1 was overexpressed in ATRT patient samples and
                      tumor cell lines. Genetic inhibition of PLK1 with shRNA
                      potently suppressed ATRT cell growth in vitro. Treatment
                      with the PLK1 inhibitor BI 6727 (Volasertib) significantly
                      decreased cell growth, inhibited clonogenic potential, and
                      induced apoptosis. BI6727 treatment led to G2-M phase
                      arrest, consistent with PLK1's role as a critical regulator
                      of mitosis. Moreover, inhibition of PLK1 by BI6727
                      suppressed the tumor-sphere formation of ATRT cells.
                      Treatment also significantly decreased levels of the DNA
                      damage proteins Ku80 and RAD51 and increased γ-H2AX
                      expression, indicating that BI 6727 can induce DNA damage.
                      Importantly, BI6727 significantly enhanced radiation
                      sensitivity of ATRT cells. In vivo, BI6727 slowed growth of
                      ATRT tumors and prolonged survival in a xenograft model.
                      PLK1 inhibition is a compelling new therapeutic approach for
                      treating ATRT, and the use of BI6727 should be evaluated in
                      clinical studies.},
      keywords     = {ATRT (Other) / Polo-like kinase 1 (Other) / SMARCB1 (Other)
                      / volasertib (Other)},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29228610},
      pmc          = {pmc:PMC5722562},
      doi          = {10.18632/oncotarget.21932},
      url          = {https://inrepo02.dkfz.de/record/181116},
}