TY  - JOUR
AU  - Logotheti, Stella
AU  - Vasilopoulos, Spyridon N
AU  - Tremi, Ioanna
AU  - Gkikoudi, Angeliki
AU  - Fragkos, Michalis
AU  - Pavlopoulou, Athanasia
AU  - Havaki, Sophia
AU  - Georgakilas, Alexandros G
TI  - The DNA Damage Response as an Auxiliary Indicator of Senescence in Cancer: A User-Friendly Toolkit of Markers and Detection Methods.
JO  - Methods in molecular biology
VL  - 2906
SN  - 1064-3745
CY  - Totowa, NJ
PB  - Humana Press
M1  - DKFZ-2025-00568
SN  - 978-1-0716-4425-6 (print)
SP  - 83-112
PY  - 2025
N1  - #EA:E041#
AB  - 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.
KW  - Humans
KW  - Cellular Senescence: genetics
KW  - DNA Damage
KW  - Neoplasms: genetics
KW  - Neoplasms: metabolism
KW  - Neoplasms: pathology
KW  - DNA Repair
KW  - Senescence-Associated Secretory Phenotype
KW  - Biomarkers, Tumor: metabolism
KW  - Biomarkers, Tumor: genetics
KW  - Cell Line, Tumor
KW  - Biomarkers
KW  - Biomarkers (Other)
KW  - DNA Damage Response (DDR) (Other)
KW  - DNA damage (Other)
KW  - Damage Response and Repair (DDR/R) (Other)
KW  - Microscopy (Other)
KW  - Senescence (Other)
KW  - Biomarkers, Tumor (NLM Chemicals)
KW  - Biomarkers (NLM Chemicals)
LB  - PUB:(DE-HGF)3 ; PUB:(DE-HGF)16
C6  - pmid:40082352
DO  - DOI:DOI:10.1007/978-1-0716-4426-3_6
UR  - https://inrepo02.dkfz.de/record/299831
ER  -