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@ARTICLE{Logotheti:299831,
      author       = {S. Logotheti$^*$ and S. N. Vasilopoulos and I. Tremi and A.
                      Gkikoudi and M. Fragkos and A. Pavlopoulou and S. Havaki and
                      A. G. Georgakilas},
      title        = {{T}he {DNA} {D}amage {R}esponse as an {A}uxiliary
                      {I}ndicator of {S}enescence in {C}ancer: {A}
                      {U}ser-{F}riendly {T}oolkit of {M}arkers and {D}etection
                      {M}ethods.},
      journal      = {Methods in molecular biology},
      volume       = {2906},
      issn         = {1064-3745},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {DKFZ-2025-00568},
      isbn         = {978-1-0716-4425-6 (print)},
      pages        = {83-112},
      year         = {2025},
      note         = {#EA:E041#},
      abstract     = {Senescence is a cellular stress response causing a stable
                      exit from the cell cycle. Limitation of cell proliferation
                      is accompanied by a variety of characteristic changes,
                      including cellular and nuclear morphological alterations,
                      chromatin rearrangements, metabolic reprogramming, nuclear
                      envelope rupture, and an immunomodulatory secretome, termed
                      senescence-associated secreted phenotype (SASP). Senescence
                      is a robust mechanism of tissue homeostasis, with crucial
                      roles in eliminating dysfunctional and/or premalignant
                      cells, and tissue repair. Activation of oncogenes triggers
                      senescence, which in turn arrests DNA-damaged cells. This
                      type of response, known as oncogene-induced senescence (OIS)
                      is a powerful barrier to oncogenesis. However, in specific
                      contexts, senescent cells support tumor progression, mainly
                      via their secretome-mediated activities. The dynamic,
                      context-dependent and ambivalent nature of senescence
                      challenges the identification, characterization, and
                      specific targeting of senescent cells for disease
                      management. Importantly, senescence is highly intertwined
                      with DNA damage response and repair (DDR/R) machinery that
                      safeguards genome integrity. DNA damage events are
                      frequently prevalent, while DDR/R signaling pathways are
                      active during cellular senescence. In this regard, it can
                      serve as an auxiliary indicator for senescent cells. In this
                      chapter, we emphasize DDR/R as a shared hallmark of cancer
                      and senescence. We provide a wieldy toolkit of experimental
                      methods for monitoring DDR-related senescence markers, and
                      we demonstrate the potential of using natural language
                      processing to extract additional DDR/R biomarkers tailored
                      to specific cancer types. Our methodologies can facilitate a
                      comprehensive study of senescence in aging and cancer.},
      keywords     = {Humans / Cellular Senescence: genetics / DNA Damage /
                      Neoplasms: genetics / Neoplasms: metabolism / Neoplasms:
                      pathology / DNA Repair / Senescence-Associated Secretory
                      Phenotype / Biomarkers, Tumor: metabolism / Biomarkers,
                      Tumor: genetics / Cell Line, Tumor / Biomarkers / Biomarkers
                      (Other) / DNA Damage Response (DDR) (Other) / DNA damage
                      (Other) / Damage Response and Repair (DDR/R) (Other) /
                      Microscopy (Other) / Senescence (Other) / Biomarkers, Tumor
                      (NLM Chemicals) / Biomarkers (NLM Chemicals)},
      cin          = {E041},
      ddc          = {570},
      cid          = {I:(DE-He78)E041-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)3 / PUB:(DE-HGF)16},
      pubmed       = {pmid:40082352},
      doi          = {DOI:10.1007/978-1-0716-4426-3_6},
      url          = {https://inrepo02.dkfz.de/record/299831},
}