Genome stability: Keeping the centrosome cycle on track

Genomic instability is characteristic of cancer cells, and promotes the accumulation of genetic lesions that contribute to their neoplastic progression. There are at least two general mechanisms by which cells exhibiting genomic instability can depart from the diploid state. One involves DNA damage from high levels of translocations, gene amplification or other chromosomal anomalies. The other involves chromosome segregation errors, probably arising from defective mitotic spindles, leading to extensive aneuploidy or even tetraploidy. A compelling argument has been made that cells with defective checkpoint controls on the cell cycle are unable to respond to DNA damage or spindle defects, thereby allowing the cells to proceed through the cell cycle while retaining the damage, possibly in consequence entering an aberrant state [1,2].