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@ARTICLE{Belenki:300198,
      author       = {D. Belenki and P. Richter-Pechanska and Z. Shao and A.
                      Bhattacharya and A. Lau and J. A. Nabuco Leva Ferreira de
                      Freitas and G. Kandler and T. P. Hick and X. Cai and E.
                      Scharnagl and A. Bittner and M. Schönlein and J. Kase and
                      K. Pardon and B. Brzezicha and N. Thiessen and O. Bischof
                      and J. R. Dörr and M. Reimann and M. Milanovic$^*$ and J.
                      Du and Y. Yu and B. Chapuy and S. Lee and U. Leser and C.
                      Scheidereit and J. Wolf and D. N. Y. Fan$^*$ and C. A.
                      Schmitt$^*$},
      title        = {{S}enescence-associated lineage-aberrant plasticity evokes
                      {T}-cell-mediated tumor control.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00675},
      pages        = {3079},
      year         = {2025},
      abstract     = {Cellular senescence is a stress-inducible state switch
                      relevant in aging, tumorigenesis and cancer therapy. Beyond
                      a lasting arrest, senescent cells are characterized by
                      profound chromatin remodeling and transcriptional
                      reprogramming. We show here myeloid-skewed aberrant lineage
                      plasticity and its immunological ramifications in
                      therapy-induced senescence (TIS) of primary human and murine
                      B-cell lymphoma. We find myeloid transcription factor (TF)
                      networks, specifically AP-1-, C/EBPβ- and PU.1-governed
                      transcriptional programs, enriched in TIS but not in equally
                      chemotherapy-exposed senescence-incapable cancer cells.
                      Dependent on these master TF, TIS lymphoma cells adopt a
                      lineage-promiscuous state with properties of
                      monocytic-dendritic cell (DC) differentiation. TIS lymphoma
                      cells are preferentially lysed by T-cells in vitro, and mice
                      harboring DC-skewed Eμ-myc lymphoma experience
                      significantly longer tumor-free survival. Consistently,
                      superior long-term outcome is also achieved in diffuse large
                      B-cell lymphoma patients with high expression of a
                      TIS-related DC signature. In essence, these data demonstrate
                      a therapeutically exploitable, prognostically favorable
                      immunogenic role of senescence-dependent aberrant myeloid
                      plasticity in B-cell lymphoma.},
      keywords     = {Animals / Humans / Cellular Senescence: immunology /
                      Cellular Senescence: genetics / Mice / T-Lymphocytes:
                      immunology / Cell Lineage / Cell Differentiation / Dendritic
                      Cells: immunology / Cell Line, Tumor / Lymphoma, Large
                      B-Cell, Diffuse: immunology / Lymphoma, Large B-Cell,
                      Diffuse: genetics / Lymphoma, Large B-Cell, Diffuse:
                      pathology / Proto-Oncogene Proteins: metabolism /
                      Proto-Oncogene Proteins: genetics / CCAAT-Enhancer-Binding
                      Protein-beta: metabolism / CCAAT-Enhancer-Binding
                      Protein-beta: genetics / Gene Expression Regulation,
                      Neoplastic / Cell Plasticity / Transcription Factor AP-1:
                      metabolism / Mice, Inbred C57BL / Monocytes: immunology /
                      Monocytes: metabolism / Lymphoma, B-Cell: immunology /
                      Lymphoma, B-Cell: genetics / Female / Transcription Factors:
                      metabolism / Transcription Factors: genetics /
                      Trans-Activators / proto-oncogene protein Spi-1 (NLM
                      Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) /
                      CCAAT-Enhancer-Binding Protein-beta (NLM Chemicals) /
                      Transcription Factor AP-1 (NLM Chemicals) / Transcription
                      Factors (NLM Chemicals) / Trans-Activators (NLM Chemicals)},
      cin          = {BE01},
      ddc          = {500},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40159497},
      doi          = {10.1038/s41467-025-57429-x},
      url          = {https://inrepo02.dkfz.de/record/300198},
}