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@ARTICLE{Khalid:179901,
      author       = {U. Khalid$^*$ and M. Simovic$^*$ and L. A. Hammann$^*$ and
                      M. Iskar$^*$ and J. K. L. Wong$^*$ and R. Kumar$^*$ and M.
                      Jugold$^*$ and M. Sill$^*$ and M. Bolkestein$^*$ and T.
                      Kolb$^*$ and M. Hergt$^*$ and F. Devens$^*$ and J. Ecker$^*$
                      and M. Kool$^*$ and T. Milde$^*$ and F. Westermann$^*$ and
                      A. Benner$^*$ and J. Lewis and S. Dietrich and S. M.
                      Pfister$^*$ and P. Lichter$^*$ and M. Zapatka$^*$ and A.
                      Ernst$^*$},
      title        = {{A} synergistic interaction between {HDAC}- and {PARP}
                      inhibitors in childhood tumors with chromothripsis.},
      journal      = {International journal of cancer},
      volume       = {151},
      number       = {4},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2022-00958},
      pages        = {590-606},
      year         = {2022},
      note         = {#EA:B420#LA:B420# / 2022 Aug 15;151(4):590-606},
      abstract     = {Chromothripsis is a form of genomic instability
                      characterized by the occurrence of tens to hundreds of
                      clustered DNA double-strand breaks in a one-off catastrophic
                      event. Rearrangements associated with chromothripsis are
                      detectable in numerous tumor entities and linked with poor
                      prognosis in some of these, such as Sonic Hedgehog
                      medulloblastoma, neuroblastoma and osteosarcoma. Hence,
                      there is a need for therapeutic strategies eliminating tumor
                      cells with chromothripsis. Defects in DNA double-strand
                      break repair, and in particular homologous recombination
                      repair, have been linked with chromothripsis. Targeting DNA
                      repair deficiencies by synthetic lethality approaches, we
                      performed a synergy screen using drug libraries (n = 375
                      compounds, 15 models) combined with either a PARP inhibitor
                      or cisplatin. This revealed a synergistic interaction
                      between the HDAC inhibitor romidepsin and PARP inhibition.
                      Functional assays, transcriptome analyses and in vivo
                      validation in patient-derived xenograft mouse models
                      confirmed the efficacy of the combinatorial treatment.},
      keywords     = {HDAC inhibitor (Other) / PARP inhibitor (Other) /
                      chromothripsis (Other) / synergy (Other) / synthetic
                      lethality (Other)},
      cin          = {B420 / B060 / W240 / B062 / HD01 / B310 / B087 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)B420-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)W240-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)B310-20160331 /
                      I:(DE-He78)B087-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35411591},
      doi          = {10.1002/ijc.34027},
      url          = {https://inrepo02.dkfz.de/record/179901},
}