th microsatellite instability which were tested had a normal checkpoint response, with an accumulation of cells which had condensed chromosomes characteristic of sustained mitotic block. The response of these cells was characteristic of cells with intact mitotic checkpoints, and similar to the response observed in normal human fibroblasts.
The cell lines with chromosomal instability acted differently. They showed an abnormal response, with fewer mitotic cells and no clear peak in mitotic activity. These differences in cell responses were also seen when a different drug, colcemid, and also with a drug that blocks microtubules through a different mechanism.
These results showed that tumor cells with chromosomal instabilities were defective in a well-defined mitotic checkpoint and had a phenotype similar to that seen in yeast cells with genetic alterations of mitotic checkpoint genes, such as BUBI cells. The data are consistent with the possibility that aneuploidy
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