Abstract
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. 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. 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.
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