Cancer drug may point to new treatment for chronic nerve pain

A protein associated with cancer may also help drive chronic nerve pain, according to research from the United States. Blocking that protein reduced pain sensitivity in preclinical models.

The study focused on neuropathic pain, which results from nerve damage and can persist for long periods. Existing painkillers often provide limited relief, prompting researchers at the University of Texas MD Anderson Cancer Center to examine the mechanisms behind the condition.

They first investigated NMDA receptors, protein channels in the brain and spinal cord that help nerve cells transmit signals. After nerve damage, these receptors can become overactive and amplify pain signals. The researchers then examined whether BRAF helped trigger that excessive activity.

In a preclinical nerve-injury model, BRAF moved from peripheral sensory nerve cells to nerve endings in the spinal cord. There, it activated molecular signaling that increased NMDA receptor activity. The team also observed a relationship between proteins involved in BRAF signaling and NMDA receptors in human spinal cord tissue samples.

Researchers then tested drugs that could interfere with the pathway. Vemurafenib, a BRAF inhibitor already used as a cancer drug, reduced the models’ sensitivity to touch, pressure and heat. The researchers said the work identifies a possible treatment direction, but it does not yet show that the drug can treat neuropathic pain in people. Further studies must determine suitable doses, delivery methods and potential side effects, as well as why BRAF moves to the spinal cord after nerve injury.