The current paradigm for bone metastasis is that there is a mutual interaction between osteoclasts and cancer cells, known as the tumor/bone vicious cycle. This model is based largely on findings in immune compromised animals showing amelioration of bone metastases by targeting the osteoclasts. Thus, osteoclast inhibitors are the standard of care in breast cancer bone metastasis. However, clinical studies demonstrate only a 28 % reduction in skeletal-related events in patients with bone metastases treated with bisphosphonates, and currently, there is limited evidence supporting anti-resorptive therapies in reducing the overall incidence of bone metastasis or extending survival. These data indicate that other cells, in addition to the osteoclasts, control tumor growth in bone. This review will discuss the role of the osteoclast, and then focus on additional cellular players, thus expanding the model of bone metastasis pathophysiology to include immune and stromal components.
- Bone metastases
- T cells