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@ARTICLE{Vogler:300099,
      author       = {M. Vogler$^*$ and Y. Braun and V. M. Smith and M.-A.
                      Westhoff and R. S. Pereira and N. M. Pieper and M. Anders
                      and M. Callens and T. Vervliet and M. Abbas and S. Macip and
                      R. Schmid and G. Bultynck and M. J. Dyer},
      title        = {{T}he {BCL}2 family: from apoptosis mechanisms to new
                      advances in targeted therapy.},
      journal      = {Signal transduction and targeted therapy},
      volume       = {10},
      number       = {1},
      issn         = {2095-9907},
      address      = {London},
      publisher    = {Macmillan Publishers, part of Springer Nature},
      reportid     = {DKFZ-2025-00599},
      pages        = {91},
      year         = {2025},
      abstract     = {The B cell lymphoma 2 (BCL2) protein family critically
                      controls apoptosis by regulating the release of cytochrome c
                      from mitochondria. In this cutting-edge review, we summarize
                      the basic biology regulating the BCL2 family including
                      canonical and non-canonical functions, and highlight
                      milestones from basic research to clinical applications in
                      cancer and other pathophysiological conditions. We review
                      laboratory and clinical development of BH3-mimetics as well
                      as more recent approaches including proteolysis targeting
                      chimeras (PROTACs), antibody-drug conjugates (ADCs) and
                      tools targeting the BH4 domain of BCL2. The first
                      BCL2-selective BH3-mimetic, venetoclax, showed remarkable
                      efficacy with manageable toxicities and has transformed the
                      treatment of several hematologic malignancies. Following its
                      success, several chemically similar BCL2 inhibitors such as
                      sonrotoclax and lisaftoclax are currently under clinical
                      evaluation, alone and in combination. Genetic analysis
                      highlights the importance of BCL-XL and MCL1 across
                      different cancer types and the possible utility of
                      BH3-mimetics targeting these proteins. However, the
                      development of BH3-mimetics targeting BCL-XL or MCL1 has
                      been more challenging, with on-target toxicities including
                      thrombocytopenia for BCL-XL and cardiac toxicities for MCL1
                      inhibitors precluding clinical development. Tumor-specific
                      BCL-XL or MCL1 inhibition may be achieved by novel targeting
                      approaches using PROTACs or selective drug delivery
                      strategies and would be transformational in many subtypes of
                      malignancy. Taken together, we envision that the targeting
                      of BCL2 proteins, while already a success story of
                      translational research, may in the foreseeable future have
                      broader clinical applicability and improve the treatment of
                      multiple diseases.},
      subtyp        = {Review Article},
      keywords     = {Humans / Proto-Oncogene Proteins c-bcl-2: antagonists $\&$
                      inhibitors / Proto-Oncogene Proteins c-bcl-2: genetics /
                      Apoptosis: drug effects / Apoptosis: genetics / Neoplasms:
                      drug therapy / Neoplasms: genetics / Neoplasms: pathology /
                      Neoplasms: metabolism / Molecular Targeted Therapy /
                      Sulfonamides: therapeutic use / Sulfonamides: pharmacology /
                      Myeloid Cell Leukemia Sequence 1 Protein: genetics / Myeloid
                      Cell Leukemia Sequence 1 Protein: antagonists $\&$
                      inhibitors / Myeloid Cell Leukemia Sequence 1 Protein:
                      metabolism / Bridged Bicyclo Compounds, Heterocyclic:
                      therapeutic use / bcl-X Protein: genetics / bcl-X Protein:
                      antagonists $\&$ inhibitors / Proto-Oncogene Proteins
                      c-bcl-2 (NLM Chemicals) / BCL2 protein, human (NLM
                      Chemicals) / Sulfonamides (NLM Chemicals) / venetoclax (NLM
                      Chemicals) / Myeloid Cell Leukemia Sequence 1 Protein (NLM
                      Chemicals) / Bridged Bicyclo Compounds, Heterocyclic (NLM
                      Chemicals) / MCL1 protein, human (NLM Chemicals) / bcl-X
                      Protein (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:40113751},
      pmc          = {pmc:PMC11926181},
      doi          = {10.1038/s41392-025-02176-0},
      url          = {https://inrepo02.dkfz.de/record/300099},
}