Julie Rhoads Sterling, PhD

Our research focuses tumors (including breast, prostate, lung, myeloma, oral cancer, and others) that metastasize or invade into the bone and induce subsequent changes in the bone that lead to increased fracture rates and pain in patients. Unfortunately, there are no cures for tumors once they have established in bone. We study the mechanisms that regulate tumor establishment in bone and bone destruction, which requires a blend of molecular biology, engineering, and pre-clinical models. These techniques together have helped us better understand tumor-induced bone disease and have allowed us to begin testing promising therapeutics in small animal models of tumor-induced bone disease. Specifically, our previous studies have demonstrated that the expression of Gli2, a transcription factor, is strongly correlated with tumor cells that induce bone destruction. We have further shown that the physical and cellular components of the bone and bone marrow can alter gene expression and tumor behavior. Our current work is further exploring how complex interactions with the bone/bone marrow contribute to disease, and have begun testing inhibitor of signaling pathways important for tumor interactions with the bone microenvironment.