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Nearly all human gliomas exhibit alterations in one of three genetic loci governing G 1  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.

genes and development

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