Neuroimmune mechanisms in cancer pain

被引:25
作者
Brown, Matthew R. D. [1 ,2 ]
Ramirez, Juan D. [3 ]
机构
[1] Royal Marsden Hosp, London SW3 6JJ, England
[2] Inst Canc Res, Sutton, Surrey, England
[3] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Clin Neurosci, Oxford OX3 9DU, England
关键词
cancer; graft-versus-host disease; neuroimmune; pain; VERSUS-HOST-DISEASE; INDUCED PERIPHERAL NEUROPATHY; INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY; LANGERHANS CELL ACTIVATION; DORSAL-ROOT GANGLIA; INDUCED BONE PAIN; CENTRAL SENSITIZATION; MOLECULAR-MECHANISMS; NEURONAL PLASTICITY; POSTSURGICAL PAIN;
D O I
10.1097/SPC.0000000000000140
中图分类号
R19 [保健组织与事业(卫生事业管理)];
学科分类号
摘要
Purpose of review The current review provides a summary of recent advances in our understanding of the neuroimmune interactions which influence the development of pain associated with cancer. Recent findings Common signalling pathways, mediators and immune cell types are involved in the generation of pain as a result of both cancer and its treatment. Distinct alterations in central and peripheral neuronal function occur in multiple forms of cancer pain. Other more unusual neuroimmune processes such as graft-versus-host disease may cause cancer pain. Summary Identification of the cellular processes which underlie the generation of cancer pain provide potential novel targets for drug development and may eventually lead to improved pain management for cancer patients.
引用
收藏
页码:103 / 111
页数:9
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