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@ARTICLE{Khn:301475,
      author       = {M. W. M. Kühn$^*$ and N. Pemmaraju and F. H. Heidel},
      title        = {{T}he evolving landscape of epigenetic target molecules and
                      therapies in myeloid cancers: focus on acute myeloid
                      leukemia and myeloproliferative neoplasms.},
      journal      = {Leukemia},
      volume       = {39},
      number       = {8},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01017},
      pages        = {1824-1837},
      year         = {2025},
      note         = {39(8):1824-1837},
      abstract     = {Research on myeloid neoplasms, a field that has been
                      driving scientific advances in cancer for over 50 years, has
                      yielded many discoveries that have fundamentally reshaped
                      our understanding of cancer biology. These insights, often
                      the product of leukemia research, have been instrumental in
                      developing more mechanism-based treatments in the early
                      2000s [1]. Recognizing epigenetic dysregulation as a common
                      disease mechanism in myeloid cancers has been groundbreaking
                      regarding recent treatment developments that exploit
                      chromatin-based oncogenic mechanisms. In the case of acute
                      myeloid leukemia (AML), sequencing studies aimed at
                      assessing the complement of genetic alterations demonstrated
                      that more than $60\%$ of AML cases harbored disease-driving
                      mutations in epigenetic regulators. This high prevalence
                      underscores the importance of epigenetic dysregulation in
                      AML pathogenesis [2, 3]. Chromatin regulators commonly
                      control disease-specific transcriptional programs, making
                      them attractive therapeutic targets to manipulate neoplastic
                      gene expression programs, particularly in myeloid neoplasms.
                      Several drugs targeting epigenetic mechanisms and exploiting
                      myeloid disease-specific dependencies have recently been
                      approved for treating myeloid neoplasms. Many additional
                      drugs are currently being investigated in clinical trials,
                      and numerous new compound developments are being studied in
                      preclinical studies. This manuscript will review (1)
                      chromatin-based disease mechanisms, such as DNA methylation,
                      chromatin regulatory complexes, and histone modifications,
                      currently investigated for therapeutic exploitation in
                      myeloid malignancies, and (2) therapeutic developments
                      already approved or investigated for treating these
                      diseases.},
      subtyp        = {Review Article},
      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:40374809},
      doi          = {10.1038/s41375-025-02639-x},
      url          = {https://inrepo02.dkfz.de/record/301475},
}