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@ARTICLE{Rausch:284610,
      author       = {J. Rausch$^*$ and E. Ullrich$^*$ and M. W. M. Kühn$^*$},
      title        = {{E}pigenetic targeting to enhance acute myeloid
                      leukemia-directed immunotherapy.},
      journal      = {Frontiers in immunology},
      volume       = {14},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2023-02030},
      pages        = {1269012},
      year         = {2023},
      abstract     = {AML is a malignant disease of hematopoietic progenitor
                      cells with unsatisfactory treatment outcome, especially in
                      patients that are ineligible for intensive chemotherapy.
                      Immunotherapy, comprising checkpoint inhibition, T-cell
                      engaging antibody constructs, and cellular therapies, has
                      dramatically improved the outcome of patients with solid
                      tumors and lymphatic neoplasms. In AML, these approaches
                      have been far less successful. Discussed reasons are the
                      relatively low mutational burden of AML blasts and the
                      difficulty in defining AML-specific antigens not expressed
                      on hematopoietic progenitor cells. On the other hand,
                      epigenetic dysregulation is an essential driver of
                      leukemogenesis, and non-selective hypomethylating agents
                      (HMAs) are the current backbone of non-intensive treatment.
                      The first clinical trials that evaluated whether HMAs may
                      improve immune checkpoint inhibitors' efficacy showed modest
                      efficacy except for the anti-CD47 antibody that was
                      substantially more efficient against AML when combined with
                      azacitidine. Combining bispecific antibodies or cellular
                      treatments with HMAs is subject to ongoing clinical
                      investigation, and efficacy data are awaited shortly. More
                      selective second-generation inhibitors targeting specific
                      chromatin regulators have demonstrated promising preclinical
                      activity against AML and are currently evaluated in clinical
                      trials. These drugs that commonly cause leukemia cell
                      differentiation potentially sensitize AML to immune-based
                      treatments by co-regulating immune checkpoints, providing a
                      pro-inflammatory environment, and inducing (neo)-antigen
                      expression. Combining selective targeted epigenetic drugs
                      with (cellular) immunotherapy is, therefore, a promising
                      approach to avoid unintended effects and augment efficacy.
                      Future studies will provide detailed information on how
                      these compounds influence specific immune functions that may
                      enable translation into clinical assessment.},
      subtyp        = {Review Article},
      keywords     = {acute myeloid leukemia (Other) / cellular therapy (Other) /
                      checkpoint inhibition (Other) / chromatin modifiers (Other)
                      / combination therapy (Other) / epigenetics (Other) /
                      hypomethylating agents (Other) / immunotherapy (Other)},
      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:37809078},
      pmc          = {pmc:PMC10556528},
      doi          = {10.3389/fimmu.2023.1269012},
      url          = {https://inrepo02.dkfz.de/record/284610},
}