The cancer genomics field has focused on how mutations in the genome change proteins to cause cells to progress into metastatic cancers. However, new molecular profiling technologies in the past years have shown that during cancer progression thousands of genes produce abnormal forms of their proteins through a mechanism called alternative splicing. This mechanism has been found to change the activities of many proteins, including transcription factors, molecules that act as the control center for the cell. However, very little is known about how these alternative splice-driven changes in TF activity lead to cancer. Therefore, we have developed several key technologies that allow for 1) sensitive detection of the presence of cancer-specific protein forms, and 2) profiling of the deregulated activities of these protein forms. This information can be used to understand new cancer mechanisms, as well as discover new precise targets for drugs or biomarkers to better diagnose cancer.