期刊
NEUROSCIENCE BULLETIN
卷 -, 期 -, 页码 -出版社
SPRINGER
DOI: 10.1007/s12264-023-01126-6
关键词
Cancer-induced bone pain; Peripheral mechanism; Tumor microenvironment; Sensory nerve; Immunocytes
This study discusses the peripheral mechanism of Cancer-induced bone pain (CIBP), including tissue injury in the bone, changes in the tumor microenvironment, and the role of the dorsal root ganglion. The interaction between nerve-cancer cells and cancer-immunocytes in the tumor microenvironment leads to the development of CIBP.
Cancer-induced bone pain (CIBP) is a type of ongoing or breakthrough pain caused by a primary bone tumor or bone metastasis. CIBP constitutes a specific pain state with distinct characteristics; however, it shares similarities with inflammatory and neuropathic pain. At present, although various therapies have been developed for this condition, complete relief from CIBP in patients with cancer is yet to be achieved. Hence, it is urgent to study the mechanism underlying CIBP to develop efficient analgesic drugs. Herein, we focused on the peripheral mechanism associated with the initiation of CIBP, which involves tissue injury in the bone and changes in the tumor microenvironment (TME) and dorsal root ganglion. The nerve-cancer and cancer-immunocyte cross-talk in the TME creates circumstances that promote tumor growth and metastasis, ultimately leading to CIBP. The peripheral mechanism of CIBP and current treatments as well as potential therapeutic targets are discussed in this review.
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