Cytokines shape chemotherapy-induced and ‘bystander' senescence
Year: 2010
Type: editorial
Abstract: The permanent proliferation arrest, distended morphology and other phenotypic features characteristic of cellular senescence can be triggered by telomere attrition (replicative senescence) and various stresses such as activated oncogenes or genotoxic treatments (premature senescence). Physiological relevance of cellular senescence is apparent from its emerging roles in aging, in tumor pathogenesis as an inducible barrier to tumor progression, and in response to radiotherapy and chemotherapy [1]. Mechanistically, senescence induction and maintenance involve the major tumor suppressor pathways of pRB and p53, and persistent signaling of the DNA damage response (DDR) machinery [1]. An integral part of DNA damage signaling and senescence is the activation of a complex
Source: Aging
Authors: Zdenek Hodny, Sona Hubackova, Jiri Bartek
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W118607157