The current standard of care for bone metastasis is therapies targeting the cells that degrade bone. These cells are directed by cancer cells to degrade bone in order to release pro-tumorigenic growth factors stored within the skeletal extracellular matrix. These therapies are not curative and do not halt metastasis-mediated bone degradation, indicating additional factors contribute to bone degradation. My research program focuses on the skeletal mechanical environment and its regulation of cancer. Specifically, I will investigate 1) the skeleton’s mechanical environment and its regulation of the remodeling process, and 2) the role of osteoblastic cells, which comprise the principal sensor and effector cells of mechanical cues, in metastatic processes. My long-term goal is to identify novel therapeutic targets for treating and preventing bone metastases as well as cancer-associated reductions in bone strength. My experimental approach uses novel in vivo and in vitro mechanical loading model systems to correlate cellular function with cancer pathogenesis, tissue-level changes in tumor burden, and skeletal tissue strength.