Cancer is the second leading cause of death in the United States after heart disease, with over half a million cancer-related deaths per year. When a cancer becomes highly aggressive, it may undergo metastasis and spread to other areas of the body which were previously free of cancer cells. Metastasis is responsible for 90% of cancer-related deaths, and cancer cells at this stage often develop high resistance to conventional therapies making them much harder to treat. Therefore, there is an urgent need for new treatments that can target advanced cancers. A breakthrough in the development of anti-cancer therapies was the development of Gleevec, an inhibitor of the BCR-Abl protein that causes chronic myelogenous leukemia (CML). More recently, Gleevec has been used clinically to treat other types of cancer, including prostate cancer, but with mixed results, or even worsening patient outcomes in some cases. To gain insight into how Gleevec may affect the behavior of solid tumor cells, we used time-lapse video-microscopy and image analysis software to measure the motility of Gleevec-treated prostate cancer cells, as well as cells treated with the Abl kinase activator, DPH. We observed that Gleevec appears to increase the migration speed of the cells, while DPH slows them down. The increased tumor cell migration caused by Gleevec may therefore help to explain the failure of Gleevec in prostate cancer trials. Our data suggest that, unlike the BCR-Abl fusion protein in CML, wild type Abl proteins may play anti-metastatic roles in prostate cancer possibly by diminishing the migration of the cells. Understanding the different roles Abl proteins may have in different cancers will be key for the developing Abl kinase-targeted anti-cancer therapies.