Mechanism of Cancer Pain

  1. Brian L. Schmidt1,
  2. Darryl T. Hamamoto2,
  3. Donald A. Simone2 and
  4. George L. Wilcox3
  1. 1 Department of Oral and Maxillofacial Surgery, School of Dentistry, University of California San Francisco
  2. 2 Department of Diagnostic and Biological Sciences, School of Dentistry and Center for Pain Research, University of Minnesota, Minneapolis
  3. 3 Departments of Neuroscience, Pharmacology and Dermatology, Center for Pain Research and Medical School, University of Minnesota, Minneapolis


Ongoing and breakthrough pain is a primary concern for the cancer patient. Although the etiology of cancer pain remains unclear, animal models of cancer pain have allowed investigators to unravel some of the cancer-induced neuropathologic processes that occur in the region of tumor growth and in the dorsal horn of the spinal cord. Within the cancer microenvironment, cancer and immune cells produce and secrete mediators that activate and sensitize primary afferent nociceptors. Pursuant to these peripheral changes, nociceptive secondary neurons in spinal cord exhibit increased spontaneous activity and enhanced responsiveness to three modes of noxious stimulation: heat, cold, and mechanical stimuli. As our understanding of the peripheral and central mechanisms that underlie cancer pain improves, targeted analgesics for the cancer patient will likely follow.

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