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@ARTICLE{Scheich:278346,
      author       = {S. Scheich and J. Chen and J. Liu and F. Schnütgen$^*$ and
                      J. C. Enssle and M. Ceribelli and C. J. Thomas and J. Choi
                      and V. Morris and T. Hsiao and H. Nguyen and B. Wang and A.
                      Bolomsky and J. D. Phelan and S. Corcoran and H. Urlaub and
                      R. M. Young and B. Häupl$^*$ and G. W. Wright and D. W.
                      Huang and Y. Ji and X. Yu and W. Xu and Y. Yang and H. Zhao
                      and J. Muppidi and K.-T. Pan and T. Oellerich$^*$ and L. M.
                      Staudt},
      title        = {{T}argeting {N}-linked {G}lycosylation for the {T}herapy of
                      {A}ggressive {L}ymphomas.},
      journal      = {Cancer discovery},
      volume       = {13},
      number       = {8},
      issn         = {2159-8274},
      address      = {Philadelphia, Pa.},
      reportid     = {DKFZ-2023-01603},
      pages        = {1862 - 1883},
      year         = {2023},
      abstract     = {Diffuse large B-cell lymphoma (DLBCL) can be subdivided
                      into the activated B-cell (ABC) and germinal center B
                      cell-like (GCB) subtypes. Self-antigen engagement of B-cell
                      receptors (BCR) in ABC tumors induces their clustering,
                      thereby initiating chronic active signaling and activation
                      of NF-κB and PI3 kinase. Constitutive BCR signaling is
                      essential in some GCB tumors but primarily activates PI3
                      kinase. We devised genome-wide CRISPR-Cas9 screens to
                      identify regulators of IRF4, a direct transcriptional target
                      of NF-κB and an indicator of proximal BCR signaling in ABC
                      DLBCL. Unexpectedly, inactivation of N-linked protein
                      glycosylation by the oligosaccharyltransferase-B (OST-B)
                      complex reduced IRF4 expression. OST-B inhibition of BCR
                      glycosylation reduced BCR clustering and internalization
                      while promoting its association with CD22, which attenuated
                      PI3 kinase and NF-κB activation. By directly interfering
                      with proximal BCR signaling, OST-B inactivation killed
                      models of ABC and GCB DLBCL, supporting the development of
                      selective OST-B inhibitors for the treatment of these
                      aggressive cancers.DLBCL depends on constitutive BCR
                      activation and signaling. There are currently no
                      therapeutics that target the BCR directly and attenuate its
                      pathologic signaling. Here, we unraveled a therapeutically
                      exploitable, OST-B-dependent glycosylation pathway that
                      drives BCR organization and proximal BCR signaling. This
                      article is highlighted in the In This Issue feature, p.
                      1749.},
      keywords     = {Humans / NF-kappa B: metabolism / Glycosylation / Signal
                      Transduction / Lymphoma, Large B-Cell, Diffuse: drug therapy
                      / Lymphoma, Large B-Cell, Diffuse: genetics / Lymphoma,
                      Large B-Cell, Diffuse: metabolism / Phosphatidylinositol
                      3-Kinases: metabolism / Cell Line, Tumor / NF-kappa B (NLM
                      Chemicals) / Phosphatidylinositol 3-Kinases (NLM Chemicals)},
      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:37141112},
      doi          = {10.1158/2159-8290.CD-22-1401},
      url          = {https://inrepo02.dkfz.de/record/278346},
}