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@ARTICLE{Ng:283179,
      author       = {M. Ng and L. Verboon$^*$ and H. Issa$^*$ and R.
                      Bhayadia$^*$ and M. W. Vermunt$^*$ and R. Winkler$^*$ and L.
                      Schüler$^*$ and O. Alejo and K. Schuschel$^*$ and E.
                      Regenyi and D. Borchert and M. Heuser and D. Reinhardt and
                      M.-L. Yaspo and D. Heckl and J.-H. Klusmann$^*$},
      title        = {{M}yeloid leukemia vulnerabilities embedded in long
                      noncoding {RNA} locus {MYNRL}15.},
      journal      = {iScience},
      volume       = {26},
      number       = {10},
      issn         = {2589-0042},
      address      = {St. Louis},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-01958},
      pages        = {107844},
      year         = {2023},
      abstract     = {The noncoding genome presents a largely untapped source of
                      new biological insights, including thousands of long
                      noncoding RNA (lncRNA) loci. While lncRNA dysregulation has
                      been reported in myeloid malignancies, their functional
                      relevance remains to be systematically interrogated. We
                      performed CRISPRi screens of lncRNA signatures from normal
                      and malignant hematopoietic cells and identified MYNRL15 as
                      a myeloid leukemia dependency. Functional dissection
                      suggests an RNA-independent mechanism mediated by two
                      regulatory elements embedded in the locus. Genetic
                      perturbation of these elements triggered a long-range
                      chromatin interaction and downregulation of leukemia
                      dependency genes near the gained interaction sites, as well
                      as overall suppression of cancer dependency pathways. Thus,
                      this study describes a new noncoding myeloid leukemia
                      vulnerability and mechanistic concept for myeloid leukemia.
                      Importantly, MYNRL15 perturbation caused strong and
                      selective impairment of leukemia cells of various genetic
                      backgrounds over normal hematopoietic stem and progenitor
                      cells in vitro, and depletion of patient-derived xenografts
                      in vivo.},
      keywords     = {Biochemistry (Other) / Cancer (Other)},
      cin          = {FM01},
      ddc          = {050},
      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:37766974},
      pmc          = {pmc:PMC10520325},
      doi          = {10.1016/j.isci.2023.107844},
      url          = {https://inrepo02.dkfz.de/record/283179},
}