Aneuploidy is a major contributing factor to metastatic progression, and is found in ninety percent of solid cancerous tumors.  For a diploid cell to become an colony of aneuploid tumor cells, the cell must both (1) mis-segregate a chromosome and (2) avoid the p53-dependent cell cycle arrest that is normally triggered in response to inadvertently becoming aneuploid.  I am actively examining how somatic cells both regulate chromosome segregation and trigger p53 accumulation when chromosomes mis-segregate.  This work involves identifying and characterizing cancer-associated mutations that impair these two processes.  I have considerable expertise in the fields of cell biology, mitosis and cell cycle, quantitative fluorescence microscopy and membrane biophysics.