Senescence in cancer: Hallmarks, paradoxes, and therapeutic promise.
2/5 보강
OpenAlex 토픽 ·
Telomeres, Telomerase, and Senescence
PARP inhibition in cancer therapy
Epigenetics and DNA Methylation
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Cellular senescence is a conserved stress-responsive program defined by durable proliferative arrest and extensive remodeling of chromatin, metabolism, intercellular signaling, and immune interactions
APA
Clemens Hinterleitner, Hailey Goldberg, et al. (2026). Senescence in cancer: Hallmarks, paradoxes, and therapeutic promise.. Cell, 189(8), 2357-2378. https://doi.org/10.1016/j.cell.2026.03.005
MLA
Clemens Hinterleitner, et al.. "Senescence in cancer: Hallmarks, paradoxes, and therapeutic promise.." Cell, vol. 189, no. 8, 2026, pp. 2357-2378.
PMID
41935528 ↗
Abstract 한글 요약
Cellular senescence is a conserved stress-responsive program defined by durable proliferative arrest and extensive remodeling of chromatin, metabolism, intercellular signaling, and immune interactions. Initially described as a barrier to unlimited cell division, senescence is now recognized as a pleiotropic and heterogeneous biological process with roles in development, tissue repair, immune surveillance, tumor suppression, aging, fibrosis, and cancer progression. Despite its broad relevance, senescence remains challenging to define operationally, as its molecular features, functional outputs, and physiological consequences vary across cell types, tissues, and stimuli. This review summarizes core hallmarks of senescence while synthesizing how these features are differentially engaged, diversified, and repurposed across biological contexts. Focusing on cancer, we discuss how senescence influences tumor initiation, evolution, and therapeutic response through both cell-intrinsic and microenvironmental mechanisms. We further evaluate emerging strategies to therapeutically modulate senescence, highlighting both opportunities and unresolved challenges for precision intervention.
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