Abstract
Most cancer patients experience severe pain during their disease course, and the management of cancer pain is a major challenge for patients and the healthcare team. Many diverse translational models of cancer pain in recent years have improved our understanding of cancer-related pain. Cancer and associated cells in the cancer microenvironment may release various peripheral mediators, including ATP, formaldehyde, protons, proteases, endothelin, bradykinin, TNF and NGF, that result in the activation and/or sensitization of peripheral and central neurons, that contribute to the clinical manifestations of cancer-related pain. Identification of these mediators and the peripheral and central mechanisms by which they contribute to cancer-related pain may provide novel therapeutic targets to alleviate cancer patient suffering.
Acknowledgements
The author wishes to thank BJ Sessle for his expert review of the manuscript.
Financial & competing interests disclosure
This work was supported by a grant from the Bertha Rosenstadt Endowment. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.