title: Forging a signature of in vivo senescence.
abstract: 'Cellular senescence', a term originally defining the characteristics of cultured cells that exceed their replicative limit, has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. Proposed relationships between cellular senescence, tumour suppression, loss of tissue regenerative capacity and ageing suffer from lack of uniform definition and consistently applied criteria. Here, we highlight caveats in interpreting the importance of suboptimal senescence-associated biomarkers, expressed either alone or in combination. We advocate that more-specific descriptors be substituted for the now broadly applied umbrella term 'senescence' in defining the suite of diverse physiological responses to cellular stress.
authors.affiliation: Department of Medicine and Genetics and The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7295, USA.
authors.forename: Norman E
authors.initials: NE
authors.lastname: Sharpless
authors.affiliation: Department of Tumor Cell Biology and The Howard Hughes Medical Institute, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA.
authors.forename: Charles J
authors.initials: CJ
authors.lastname: Sherr
mesh_terms: D000818:Animals; D015415:Biomarkers; D002453:Cell Cycle; D016922:Cellular Senescence; D050762:Cyclin-Dependent Kinase Inhibitor p15 / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000502:physiology; D004249:DNA Damage; D019942:Genes, p16; D006801:Humans; D059506:Telomere Shortening; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
chemical_list: D015415:Biomarkers; C493956:CDKN1A protein, human; D050762:Cyclin-Dependent Kinase Inhibitor p15; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53