'Neuroinvasion' May Impact Cancer Pain, Progression
Reciprocal relationship between cancer and neurons at play in tumor proliferation and pain sensitization.
PALM SPRINGS, Calif. — New discoveries about the ability of cancer cells to invade along nerves, a process dubbed “neuroinvasion,” is shedding new light on the etiology of cancer pain, disease progression, and mortality.
Compared with inflammatory and neuropathic pain, cancer pain is associated with distinct set of neurochemcial changes in the spinal cord and sensory neurons, according to a speaker at the 2015 American Pain Society Annual Meeting.
“We now recognize that cancers and neurons act reciprocally on each other,” said Brian L. Schmidt, DDS, MD, PhD, a symposium speaker and professor at New York University College of Dentistry and School of Medicine.
During the symposium, Schmidt and Brian M. Davis, professor of neurobiology and medicine at the University of Pittsburgh School of Medicine, explained how the nerve itself is a facilitator of “adverse cancer behavior,” and how interactions between nerves and tumors contribute to increased pain sensitization.
“Tumors express nerve growth factor receptors and their ligands, both of which can interact with sensory fibers to cause sensitization and pain,” Davis said. “Once the tumor cell is in the nerve it can divide and grow, directly causing nerve damage and inciting neuropathic pain.”
In addition to contributing significantly to cancer pain, the researchers believe that cancer progression depends largely on nerve activity.
Molecules released by sensory neurons can promote tumorigenesis in the tumor microenvironment, they explained, or may directly interact with cancer stem cells to accelerate disease.
“In recent studies, tumors did not grow if they could not interact with nerves,” Davis said. “Further, nerves play a role in metastasis by allowing cancer cells to migrate along them to reach other organs. This usually is associated with poor prognosis.”
A large part of the difficulty healthcare providers face when treating cancer pain stems from heterogeneity at the genomic level, Schmidt explained. He advocated for more multidisciplinary research to study the cancer pain at the molecular, preclinical, and clinical levels.
“Future research might conclude that pharmacologic and nonpharmacologic antagonism of mechanisms in the neurosensory system and mechanisms integral to cancer proliferation are required to achieve improved relief of cancer pain,” Schmidt said.