Author Correction: Mutational signatures reveal the role of RAD52 in p53-independent p21-driven genomic instability

Galanos, Panagiotis; Pappas, George D.; Polyzos, Alexander; Kotsinas, Athanassios; Svolaki, Ioanna; Giakoumakis, Nickolaos Nikiforos; Glytsou, Christina; Pateras, Ioannis S.; Swain, Umakanta; Souliotis, Vassilis L.; Georgakilas, Alexandros G.; Geacintov, Nicholas E.; Scorrano, Luca; Lukas, Claudia; Lukáš, Jiří; Livneh, Zvi; Lygerou, Zoi; Chowdhury, Dipanjan; Sørensen, Claus Storgaard; Bártek, Jiří; Gorgoulis, Vassilis G.

doi:10.1186/s13059-022-02678-y

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“…Mechanistically, chronic p21 WAF1/Cip1 upregulation was shown to 'saturate' the CRL4 CDT2 and SCF Skp2 ubiquitin ligase complexes, restraining turnover of the replication licensing machinery [34]. Constituent replication stress and DDR activation, in a p53-null setting, resulted eventually in a shift from RAD-51-mediated high-fidelity repair processes to RAD-52-modulated lowfidelity repair, fuelling genomic instability (Figure 4) [83]. Escape from senescence: a new player in pathology 653 Overall, our observations implied that genomic instability played a role in escape from senescence, but direct evidence was still lacking.…”

Section: K Evangelou K Belogiannis Et Almentioning

confidence: 99%

Escape from senescence: molecular basis and therapeutic ramifications

Evangelou

Belogiannis

Papaspyropoulos

et al. 2023

The Journal of Pathology

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Cellular senescence constitutes a stress response mechanism in reaction to a plethora of stimuli. Senescent cells exhibit cell‐cycle arrest and altered function. While cell‐cycle withdrawal has been perceived as permanent, recent evidence in cancer research introduced the so‐called escape‐from‐senescence concept. In particular, under certain conditions, senescent cells may resume proliferation, acquiring highly aggressive features. As such, they have been associated with tumour relapse, rendering senescence less effective in inhibiting cancer progression. Thus, conventional cancer treatments, incapable of eliminating senescence, may benefit if revisited to include senolytic agents. To this end, it is anticipated that the assessment of the senescence burden in everyday clinical material by pathologists will play a crucial role in the near future, laying the foundation for more personalised approaches. Here, we provide an overview of the investigations that introduced the escape‐from‐senescence phenomenon, the identified mechanisms, as well as the major implications for pathology and therapy. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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Section: K Evangelou K Belogiannis Et Almentioning

confidence: 99%