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Titolo:
Modeling mutations in the G(1) arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes
Autore:
Holland, EC; Hively, WP; Gallo, V; Varmus, HE;
Indirizzi:
NICHHD, Lab Cellular & Mol Neurophysiol, NIH, Bethesda, MD 20892 USA NICHHD Bethesda MD USA 20892 ol Neurophysiol, NIH, Bethesda, MD 20892 USA NCI, Div Basic Sci, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892NCI, Div Basic Sci, NIH, Bethesda, MD 20892 USA
Titolo Testata:
GENES & DEVELOPMENT
fascicolo: 23, volume: 12, anno: 1998,
pagine: 3644 - 3649
SICI:
0890-9369(199812)12:23<3644:MMITGA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-CYCLE ARREST; TUMOR SUPPRESSION; GROWTH-FACTOR; GENE; AMPLIFICATION; DELETION; LOCUS; P16; IMMORTALIZATION; GLIOBLASTOMAS;
Keywords:
G(1) arrest; CDK4 amplification; INK4a-ARF loss; glioma-genesis; mouse astrocytes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Holland, EC MD Anderson Cancer Ctr, Dept Neurosurg, Houston, TX 77030 USA MD Anderson Cancer Ctr Houston TX USA 77030 ton, TX 77030 USA
Citazione:
E.C. Holland et al., "Modeling mutations in the G(1) arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes", GENE DEV, 12(23), 1998, pp. 3644-3649

Abstract

Nearly all human gliomas exhibit alterations in one of three genetic loci governing G(1) arrest: INK4a-ARF, CDK4, or RE. To discern the roles of CDK4amplification and INK4a-ARF loss in gliomagenesis, we compared the behavior of astrocytes lacking a functional INK4a-ARF locus with astrocytes overexpressing CDK4. Either a deficiency of p16(INK4a) and p19(ARF) or an increase in Cdk4 allows cultured astrocytes to grow without senescence. Astrocytesoverexpressing CDK4 grow more slowly than INK4a-ARF-deficient astrocytes and convert to a tetraploid state at high efficiency; in contrast, INK4a-ARF-deficient cells remain pseudodiploid, consistent with properties observed in human gliomas with corresponding lesions in these genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 22:27:02