January 12, 2005
If neoplasia often arises from a breakdown in a cell’s growth-regulating machinery, one of these malfunctioning parts can be the centrosome, the cylindrical structure that holds duplicated chromosomes in place during early mitosis. As scientists have discovered, tumor cells sometimes mistakenly produce extra centrosomes. If these extra centrosomes cluster together as one, the resulting daughter cells will likely maintain a normal complement of chromosomes. However, if the superfluous centromeres separate, they will throw off the normal spatial orientation that underlies the subsequent steps of mitosis, yielding daughter cells with an abnormal number of chromosomes, a hallmark of tumor cells. Left unanswered in these discoveries is the next critical question: What are the actual molecular mechanisms involved in inhibiting the clustering of the centrosomes? In the January 7, 2005 issue of the journal Science, NIDCR grantees provide an answer in a spindle protein called NuMA and elucidate its role in the process.