Decoding Bone Cancer Pain: Pathological Mechanisms and Targeted Interventions

Le résumé fourni par la source

Abstract Bone cancer pain (BCP) is one of the most prominent and disabling symptoms in patients with primary bone malignancies (e.g. osteosarcoma, Ewing’s sarcoma) and metastatic bone tumors (e.g. multiple myeloma), severely impacting quality of life and treatment efficacy. Conventional analgesic approaches are often limited in effectiveness or associated with significant side effects. This chapter will delve into the complex pathological mechanisms underlying the development and persistence of BCP. It will focus on elucidating the intricate interactions within the tumor micro-environment involving cancer cells, immune cells (e.g. macrophages, T cells), osteoclasts, osteoblasts, and sensory neurons. Key mechanisms include sensitization of nociceptors by allogeneic mediators (protons, nerve growth factor, cytokines, chemokines) released from tumor and stromal cells; activation of nerve terminals by factors (e.g. ATP, acid) released during bone matrix destruction; tumor and immune cell infiltration of nerves; and peripheral and central nervous system sensitization and remodeling. Building upon this mechanistic understanding, the chapter will systematically review current and emerging targeted therapeutic strategies. These include monoclonal antibodies, small molecule inhibitors, gene therapies, and neuromodulation techniques targeting key pain-signaling pathways (e.g. NGF/TrkA, GDNF, CXCL12/CXCR4, RANK/RANKL). The aim is to provide the theoretical foundation and translational insights necessary for developing more effective and better-tolerated precision treatments for BCP.

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