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@ARTICLE{Jacob:282903,
      author       = {M. Jacob and S. Wiedemann and D. Brücher and N. M. Pieper
                      and M. Birkhold and V. Särchen and J. Jeroch and M. C.
                      Demes and S. Gretser and Y. Braun and E. Gradhand and F.
                      Rothweiler and M. Michaelis and J. Cinatl and M. Vogler$^*$},
      title        = {{I}ncreased {MCL}1 dependency leads to new applications of
                      {BH}3-mimetics in drug-resistant neuroblastoma.},
      journal      = {British journal of cancer},
      volume       = {129},
      number       = {10},
      issn         = {0007-0920},
      address      = {Edinburgh},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2023-01895},
      pages        = {1667-1678},
      year         = {2023},
      note         = {2023 Nov;129(10):1667-1678},
      abstract     = {Neuroblastoma is a paediatric cancer that is characterised
                      by poor prognosis for chemoresistant disease, highlighting
                      the need for better treatment options. Here, we asked
                      whether BH3-mimetics inhibiting BCL2 proteins may eliminate
                      chemoresistant neuroblastoma cells.We utilised
                      cisplatin-adapted neuroblastoma cell lines as well as
                      patient tissues before and after relapse to study
                      alterations of BCL2 proteins upon chemoresistance.In a
                      direct comparison of cisplatin-resistant cells we identified
                      a prominent loss of sensitivity to BCL2/BCL-XL inhibitors
                      that is associated with an increase in MCL1 dependency and
                      high expression of MCL1 in patient tumour tissues. Screening
                      of FDA-approved anti-cancer drugs in chemoresistant cells
                      identified therapeutics that may be beneficial in
                      combination with the clinically tested BH3-mimetic ABT263,
                      but no synergistic drug interactions with the selective MCL1
                      inhibitor S63845. Further exploration of potential treatment
                      options for chemoresistant neuroblastoma identified
                      immunotherapy based on NK cells as highly promising, since
                      NK cells are able to efficiently kill both parental and
                      chemoresistant cells.These data highlight that the
                      application of BH3-mimetics may differ between first line
                      treatment and relapsed disease. Combination of NK cell-based
                      immunotherapy with BH3-mimetics may further increase killing
                      of chemoresistant neuroblastoma, outlining a new treatment
                      strategy for relapsed neuroblastoma.},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37723317},
      doi          = {10.1038/s41416-023-02430-8},
      url          = {https://inrepo02.dkfz.de/record/282903},
}