Abstract

Breast cancer is the most common malignancy distressing females in the world. The bone metastases are one of the most common site of disease dissemination. Up to 75% of stage IV Breast cancer patients developing skeletal metastases [1] metastatic bone disease can result in skeletal related events (SREs), including humoral hypercalcaemia of malignancy (HHM), pathological fractures, spinal cord compression, and pain [2]. The median time from bone metastases diagnosis to first SRE can be as short as 1.8 months, with the incidence of SREs growing considerably during the first 12 months following diagnosis [3]. This Bone metastases affect patient survival, movement, and quality of life by negative impact. The molecular mechanisms involved in the metastasis, colonization, and proliferation of breast cancer cells in bone are multifaceted and include crosstalk between breast cancer cells and the bone microenvironment. The capability of metastatic breast cancer cells to capture normal biological processes involved in bone remodeling is a key driver of osteolytic and osteoblastic bone lesions. As such, our understanding of how breast cancer cells manipulate normal bone remodeling pathways is essential for the development of new therapeutic agents to improve patient outcomes.