FIGURE 4.7. Schematic showing factors in bone (A) and receptors/channels expressed by nociceptors that innervate the skeleton (B) that drive bone cancer pain.

FIGURE 4.7

Schematic showing factors in bone (A) and receptors/channels expressed by nociceptors that innervate the skeleton (B) that drive bone cancer pain. A variety of cells (tumor cells, and stomal cells including inflammatory/immune cells, and osteoclasts) drive bone cancer pain (A). Nociceptors that innervate the bone use several different types of receptors to detect and transmit noxious stimuli that are produced by cancer cells, tumor-associated immune cells, or other aspects of the tumor microenvironment. There are multiple factors that may contribute to the pain associated with cancer (B). The transient receptor potential vanilloid receptor-1 (TRPV1) and acid-sensing ion channels (ASICs) detect extracellular protons produced by tumor-induced tissue damage or abnormal osteoclast mediated bone resorption. Tumor cells and associated inflammatory (immune) cells produce a variety of chemical mediators including prostaglandins (PGE2), nerve growth factor (NGF), endothelins, bradykinin, and extracellular ATP. Several of these proinflammatory mediators have receptors on peripheral terminals and can directly activate or sensitize nociceptors. NGF and its cognate receptor TrkA may serve as a master regulator of bone cancer pain by modulating the sensitivity or increasing the expression of several receptors and ion channels contributing to increased excitability of nociceptors in the vicinity of the tumor.

From: Chapter 4, Cancer Pain

Cover of Translational Pain Research
Translational Pain Research: From Mouse to Man.
Kruger L, Light AR, editors.
Boca Raton, FL: CRC Press; 2010.
Copyright © 2010 by Taylor and Francis Group, LLC.

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