Tumour-associated cell cycle defects are often mediated by alterations of incyclin-dependent kinase （CDK） activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models,mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strate- gies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for prol...
