% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Tegeder:141761,
      author       = {I. Tegeder and K. Thiel and S. Erkek$^*$ and P. Johann$^*$
                      and J. Berlandi and V. Thatikonda$^*$ and M. C. Frühwald
                      and M. Kool$^*$ and A. Jeibmann and M. Hasselblatt},
      title        = {{F}unctional relevance of genes predicted to be affected by
                      epigenetic alterations in atypical teratoid/rhabdoid
                      tumors.},
      journal      = {Journal of neuro-oncology},
      volume       = {141},
      number       = {1},
      issn         = {1573-7373},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V},
      reportid     = {DKFZ-2018-02030},
      pages        = {43-55},
      year         = {2019},
      abstract     = {Atypical teratoid/rhabdoid tumor (ATRT) is a highly
                      malignant brain tumor predominantly arising in infants.
                      Mutations of SWI/SNF chromatin remodeling complex members
                      SMARCB1/INI1 or (rarely) SMARCA4/Brg1 are the sole recurrent
                      genetic lesions. Epigenetic studies revealed a large number
                      of genes predicted to be affected by differential histone
                      modifications in ATRT, but the role of these genes in the
                      biology of ATRT remains uncertain. We therefore aimed at
                      exploring the role of these genes in the detrimental effects
                      of SMARCB1-deficiency.The functional relevance of 1083 genes
                      predicted to be affected by epigenetic alterations in ATRT
                      was examined in vivo using a Drosophila melanogaster model
                      of SMARCB1-deficiency. Human orthologues of genes whose
                      knockdown modified the phenotype in the Gal4-UAS fly model
                      were further examined in ATRT samples and SMARCB1-deficient
                      rhabdoid tumor cells.Knockdown of Snr1, the fly orthologue
                      of SMARCB1, resulted in a lethal phenotype and epigenetic
                      alterations in the fly model. The lethal phenotype was
                      shifted to later stages of development upon additional siRNA
                      knockdown of 89 of 1083 genes screened in vivo. These
                      included TGF-beta receptor signaling pathway related genes,
                      e.g. CG10348, the fly orthologue of transcriptional
                      regulator PRDM16. Subsequently, PRDM16 was found to be
                      over-expressed in ATRT samples and knockdown of PRDM16 in
                      SMARCB1-deficient rhabdoid tumor cells reduced
                      proliferation.These results suggest that a subset of genes
                      affected by differential histone modification in ATRT is
                      involved in the detrimental effects of SMARCB1-deficiency
                      and also relevant in the biology of ATRT.},
      cin          = {B062 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30446899},
      doi          = {10.1007/s11060-018-03018-6},
      url          = {https://inrepo02.dkfz.de/record/141761},
}