pproximately 1 in 4 patients with advanced breast cancer develop incurable
skeletal metastasis, which is the leading cause of breast cancer-related deaths
among women worldwide. Breast cancer metastasis is overwhelmingly osteolytic,
causing increased bone fragility and risk for fracture. Homeostatic remodeling of the
skeleton balances resorption and formation to meet structural and metabolic needs
via a feedback loop that is regulated by the prevailing mechanical environment.
Metastatic cancer cells appropriate remodeling by causing net resorption, which releases
pro-tumorigenic factors stored within the skeletal matrix. In contrast, increased
mechanical stimulation results in net bone formation. In the skeleton, cancer
cells are exposed to the mechanical environment in the skeleton, yet the role of biomechanical
loading as a regulator of tumor progression and osteolysis remains poorly
characterized. This talk will discuss novel models for investigating the effects of mechanical
loading on breast cancer bone metastasis as well as preliminary work indicating
that mechanical loading plays an inhibitory role in this context.

Read more: engineeering.dartmouth.edu/jones