LAUSR

Osteoporosis, fragility fractures, and pathologic fractures are increasingly recognized as long‐term complications in cancer survivors. Women are more susceptible to bone loss than men, and breast cancer is the most common malignancy in women. In this population, bone health is a critical concern due to both therapy‐induced bone loss and a high propensity for skeletal metastasis. Antiresorptive agents are widely used; however, their known adverse effects and limited capacity to rapidly reduce fracture risk in high‐risk individuals have led to growing support for the early use of osteoanabolic therapies. Among these, intermittent administration of parathyroid hormone [PTH (1–34)] has demonstrated clinical efficacy in reducing fracture risk by activating the PTH 1 receptor in osteoblasts. However, its safety and mechanistic relevance in the context of breast cancer remain poorly understood. This review outlines the osteoblast‐specific signaling pathways of PTH (1–34) and includes our recent research that identified p21‐activated kinase 4 as a downstream effector linking canonical cyclic adenosine monophosphate‐protein kinase A signaling to Wnt/β‐catenin activation. Additionally, it explores the potential implications of PTH (1–34) in the context of breast cancer‐related bone metastasis.