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@ARTICLE{Smith:186783,
      author       = {C. Smith and A. Touzart and M. Simonin and C. Tran-Quang
                      and G. Hypolite and M. Latiri and G. P. Andrieu and E.
                      Balducci and M.-É. Dourthe and A. Goyal$^*$ and F. Huguet
                      and A. Petit and N. Ifrah and A. Baruchel and H. Dombret and
                      E. Macintyre and C. Plass$^*$ and J. Ghysdael and N. Boissel
                      and V. Asnafi},
      title        = {{H}arnessing the {MYB}-dependent {TAL}1 5'super-enhancer
                      for targeted therapy in {T}-{ALL}.},
      journal      = {Molecular cancer},
      volume       = {22},
      number       = {1},
      issn         = {1476-4598},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DKFZ-2023-00111},
      pages        = {12},
      year         = {2023},
      abstract     = {The acquisition of genetic abnormalities engendering
                      oncogene dysregulation underpins cancer development. Certain
                      proto-oncogenes possess several dysregulation mechanisms,
                      yet how each mechanism impacts clinical outcome is unclear.
                      Using T-cell acute lymphoblastic leukemia (T-ALL) as an
                      example, we show that patients harboring 5'super-enhancer
                      (5'SE) mutations of the TAL1 oncogene identifies a specific
                      patient subgroup with poor prognosis irrespective of the
                      level of oncogene dysregulation. Remarkably, the MYB
                      dependent oncogenic 5'SE can be targeted using Mebendazole
                      to induce MYB protein degradation and T-ALL cell death. Of
                      note Mebendazole treatment demonstrated efficacy in vivo in
                      T-ALL preclinical models. Our work provides proof of concept
                      that within a specific oncogene driven cancer, the mechanism
                      of oncogene dysregulation rather than the oncogene itself
                      can identify clinically distinct patient subgroups and pave
                      the way for future super-enhancer targeting therapy.},
      keywords     = {Cancer (Other) / Oncogene (Other) / Super-enhancer (Other)
                      / Targeted therapy (Other)},
      cin          = {B370 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)B370-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36650499},
      doi          = {10.1186/s12943-022-01701-x},
      url          = {https://inrepo02.dkfz.de/record/186783},
}