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@ARTICLE{Okonechnikov:275588,
      author       = {K. Okonechnikov$^*$ and A. Camgöz$^*$ and O. Chapman and
                      S. Wani and D. E. Park and J.-M. Hübner$^*$ and A.
                      Chakraborty and M. Pagadala and R. Bump and S. Chandran and
                      K. Kraft and R. Acuna-Hidalgo and D. Reid and K. Sikkink and
                      M. Mauermann$^*$ and E. F. Juarez and A. Jenseit$^*$ and J.
                      T. Robinson and K. W. Pajtler$^*$ and T. Milde$^*$ and N.
                      Jäger$^*$ and P. Fiesel$^*$ and L. Morgan and S. Sridhar
                      and N. G. Coufal and M. Levy and D. Malicki and C. Hobbs and
                      S. Kingsmore and S. Nahas and M. Snuderl and J. Crawford and
                      R. J. Wechsler-Reya and T. B. Davidson and J. Cotter and G.
                      Michaiel and G. Fleischhack$^*$ and S. Mundlos and A.
                      Schmitt and H. Carter and K. A. Michealraj and S. A. Kumar
                      and M. D. Taylor and J. Rich and F. Buchholz$^*$ and J. P.
                      Mesirov and S. M. Pfister$^*$ and F. Ay and J. R. Dixon and
                      M. Kool$^*$ and L. Chavez},
      title        = {3{D} genome mapping identifies subgroup-specific chromosome
                      conformations and tumor-dependency genes in ependymoma.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00799},
      pages        = {2300},
      year         = {2023},
      note         = {#EA:B062#LA:B062#},
      abstract     = {Ependymoma is a tumor of the brain or spinal cord. The two
                      most common and aggressive molecular groups of ependymoma
                      are the supratentorial ZFTA-fusion associated and the
                      posterior fossa ependymoma group A. In both groups, tumors
                      occur mainly in young children and frequently recur after
                      treatment. Although molecular mechanisms underlying these
                      diseases have recently been uncovered, they remain difficult
                      to target and innovative therapeutic approaches are urgently
                      needed. Here, we use genome-wide chromosome conformation
                      capture (Hi-C), complemented with CTCF and H3K27ac ChIP-seq,
                      as well as gene expression and DNA methylation analysis in
                      primary and relapsed ependymoma tumors, to identify
                      chromosomal conformations and regulatory mechanisms
                      associated with aberrant gene expression. In particular, we
                      observe the formation of new topologically associating
                      domains ('neo-TADs') caused by structural variants,
                      group-specific 3D chromatin loops, and the replacement of
                      CTCF insulators by DNA hyper-methylation. Through inhibition
                      experiments, we validate that genes implicated by these 3D
                      genome conformations are essential for the survival of
                      patient-derived ependymoma models in a group-specific
                      manner. Thus, this study extends our ability to reveal
                      tumor-dependency genes by 3D genome conformations even in
                      tumors that lack targetable genetic alterations.},
      cin          = {B062 / HD01 / B310 / B300 / ED01 / DD01},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B310-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)ED01-20160331 / I:(DE-He78)DD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37085539},
      pmc          = {pmc:PMC10121654},
      doi          = {10.1038/s41467-023-38044-0},
      url          = {https://inrepo02.dkfz.de/record/275588},
}