| First Author | Holland EC | Year | 1998 |
| Journal | Genes Dev | Volume | 12 |
| Issue | 23 | Pages | 3644-9 |
| PubMed ID | 9851971 | Mgi Jnum | J:51558 |
| Mgi Id | MGI:1316902 | Doi | 10.1101/gad.12.23.3644 |
| Citation | Holland EC, et al. (1998) Modeling mutations in the G1 arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes. Genes Dev 12(23):3644-9 |
| abstractText | Nearly all human gliomas exhibit alterations in one of three genetic loci governing G1 arrest: INK4a-ARF, CDK4, or RB. To discern the roles of CDK4 amplification 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. Astrocytes overexpressing 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. |
