% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Eifert:278586,
      author       = {T. Eifert and C.-J. Hsu and A. L. Becker and S. Graessle
                      and A. Horne and F. Bemmann and Q. Zhang and M. Heuser and
                      V. Vasioukhin and S. Scholl and A. Hochhaus and F. Siegerist
                      and N. Endlich and L. Bullinger and S. W. Lane and S.
                      Haas$^*$ and T. M. Schnoeder and F. H. Heidel},
      title        = {{C}ell fate determinant {L}lgl1 is required for propagation
                      of acute myeloid leukemia.},
      journal      = {Leukemia},
      volume       = {37},
      number       = {10},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2023-01667},
      pages        = {2027-2035},
      year         = {2023},
      note         = {2023 Oct;37(10):2027-2035},
      abstract     = {Scribble complex proteins can influence cell fate decisions
                      and self-renewal capacity of hematopoietic cells. While
                      specific cellular functions of Scribble complex members are
                      conserved in mammalian hematopoiesis, they appear to be
                      highly context dependent. Using CRISPR/Cas9-based genetic
                      screening, we have identified Scribble complex-related
                      liabilities in AML including LLGL1. Despite its reported
                      suppressive function in HSC self-renewal, inactivation of
                      LLGL1 in AML confirms its relevant role for proliferative
                      capacity and development of AML. Its function was conserved
                      in human and murine models of AML and across various genetic
                      backgrounds. Inactivation of LLGL1 results in loss of
                      stemness-associated gene-expression including HoxA-genes and
                      induces a GMP-like phenotype in the leukemia stem cell
                      compartment. Re-expression of HoxA9 facilitates functional
                      and phenotypic rescue. Collectively, these data establish
                      LLGL1 as a specific dependency and putative target in AML
                      and emphasizes its cell-type specific functions.},
      cin          = {A010 / BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / I:(DE-He78)BE01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37587260},
      doi          = {10.1038/s41375-023-02005-9},
      url          = {https://inrepo02.dkfz.de/record/278586},
}