title: Jailbreak: oncogene-induced senescence and its evasion.
abstract: Aberrant oncogenic signals are typically counteracted by anti-proliferative mechanisms governed principally by the p53 and Rb tumour-suppressor proteins. Apoptosis is firmly established as a potent anti-proliferative mechanism to prevent tumour growth but it is only in recent years that oncogene-induced senescence has achieved similar recognition. Senescence is defined as an irreversible cell-cycle arrest suggesting that entry of oncogene-expressing cells into this static yet viable state is permanent. However, tumours do develop and express the very same oncogenes that landed them in jail. We ask whether this is because rogue incipient cancer cells find ways to escape this imposed imprisonment or otherwise entirely avoid capture by senescence gate-keepers.
authors.affiliation: Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Lab Block Level 3, Addenbrooke's Hospital, Cambridge, UK. fkem3@cam.ac.uk
authors.forename: Fiona K E
authors.initials: FK
authors.lastname: McDuff
authors.forename: Suzanne D
authors.initials: SD
authors.lastname: Turner
mesh_terms: D000818:Animals; D001343:Autophagy; D016922:Cellular Senescence; D006801:Humans; D051379:Mice; D009857:Oncogenes; D016160:Retinoblastoma Protein / Q000378:metabolism; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53