Abstract
The role of aneuploidy in tumorigenesis remains poorly understood, although the two have been known to be linked for more than 100 years. Recent studies indicate that aneuploidy can promote tumour cell growth and cell death and that the cellular outcome is dependent on the extent of aneuploidy induced. The mitotic checkpoint plays a pivotal role in the maintenance of genome stability and has been the focus of work investigating the distinct outcomes of aneuploidy. In the present article, we review the molecular mechanisms involved and discuss the potential of the mitotic checkpoint as a therapeutic target in cancer therapy.
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