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dc.contributor.authorStratton, Men_US
dc.date.accessioned2018-06-11T10:59:43Z
dc.date.issued2008-04en_US
dc.identifier4en_US
dc.identifier.citationCANCER CELL, 2008, 13 pp. 355 - 364en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1806
dc.description.abstractWe have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion. Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C). Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.en_US
dc.format.extent355 - 364en_US
dc.titleFeedback circuit among INK4 tumor suppressors constrains human glioblastoma developmenten_US
dc.typeJournal Article
rioxxterms.licenseref.startdate2008-04en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfCANCER CELLen_US
pubs.noteskeywords: COMPARATIVE GENOMIC HYBRIDIZATION; HUMAN LUNG-CANCER; ARRAY CGH DATA; GENE; REVEALS; EXPRESSION; DELETIONS; PROFILES; INACTIVATION; P18(INK4C)en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Genetic Susceptibility
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Genetic Susceptibility
pubs.volume13en_US
pubs.embargo.termsNot knownen_US
pubs.oa-locationhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292238/en_US
icr.researchteamGenetic Susceptibilityen_US
dc.contributor.icrauthorStratton, Michaelen_US


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