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@ARTICLE{Parisian:163198,
      author       = {A. D. Parisian and T. Koga and S. Miki and P. D. Johann$^*$
                      and M. Kool$^*$ and J. R. Crawford and F. B. Furnari},
      title        = {{SMARCB}1 loss interacts with neuronal differentiation
                      state to block maturation and impact cell stability.},
      journal      = {Genes $\&$ development},
      volume       = {34},
      number       = {19-20},
      issn         = {1549-5477},
      address      = {Cold Spring Harbor, NY},
      publisher    = {Laboratory Press},
      reportid     = {DKFZ-2020-01895},
      pages        = {1316-1329},
      year         = {2020},
      note         = {2020 Oct 1;34(19-20):1316-1329},
      abstract     = {Atypical teratoid rhabdoid tumors (ATRTs) are challenging
                      pediatric brain cancers that are predominantly associated
                      with inactivation of the gene SMARCB1, a conserved subunit
                      of the chromatin remodeling BAF complex, which has known
                      contributions to developmental processes. To identify
                      potential interactions between SMARCB1 loss and the process
                      of neural development, we introduced an inducible SMARCB1
                      loss-of-function system into human induced pluripotent stem
                      cells (iPSCs) that were subjected to either directed
                      neuronal differentiation or differentiation into cerebral
                      organoids. Using this system, we identified substantial
                      differences in the downstream effects of SMARCB1 loss
                      depending on differentiation state and identified an
                      interaction between SMARCB1 loss and neural differentiation
                      pressure that causes a resistance to terminal
                      differentiation and a defect in maintenance of a normal cell
                      state. Our results provide insight into how SMARCB1 loss
                      might interact with neural development in the process of
                      ATRT tumorigenesis.},
      cin          = {B062 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32912900},
      doi          = {10.1101/gad.339978.120},
      url          = {https://inrepo02.dkfz.de/record/163198},
}