Study Finds Cancer Drugs Could Offer New Hope for Chronic Nerve Pain - Video

What if a protein linked to cancer could also hold the key to treating chronic nerve pain? Researchers at The University of Texas MD Anderson Cancer Center have identified a potential new pathway involved in chronic neuropathic pain, raising the possibility that a protein already targeted in cancer treatment could eventually become a treatment target for persistent nerve pain.

Published in Science Signaling, the study found that BRAF, a protein best known for its role in cancer, may amplify pain signals following nerve injury. In preclinical models, blocking BRAF signaling reduced pain sensitivity.

Neuropathic pain can develop after nerve damage caused by injuries, diseases or treatments such as chemotherapy. Unlike temporary pain, it can persist for months or even years and is often difficult to treat.

Researchers focused on NMDA receptors, protein channels involved in communication between nerve cells. After nerve injury, excessive NMDA receptor activity can amplify pain signals and increase nervous system sensitivity.

The study found that following nerve injury, BRAF travels through sensory nerve cells toward their endings in the spinal cord. There, it appears to activate signaling that increases NMDA receptor activity, potentially contributing to persistent and amplified pain. Researchers also found evidence linking BRAF-related proteins with NMDA receptors in human spinal cord tissue.

When the team inhibited BRAF signaling in preclinical nerve-injury models, pain sensitivity decreased, suggesting that BRAF may play an active role in the biological mechanisms underlying chronic neuropathic pain.

The discovery is particularly significant because BRAF inhibitors are already used to treat certain cancers. This could provide a starting point for investigating whether existing drugs targeting the pathway might eventually be repurposed for specific forms of nerve pain.

However, the findings remain preliminary. Clinical trials are now needed to determine whether targeting BRAF can safely reduce neuropathic pain and potentially offer a treatment that addresses pain amplification at its biological source.

REFERENCE: Daozhong Jin, Hong Chen, et al.; “BRAF recruitment to spinal sensory synapses promotes neuropathic pain by potentiating transsynaptic NMDA receptor activity” 2026, Science Signaling. DOI: 10.1126/scisignal.aeh6852