Preclinical study points to cancer drugs as possible treatments for chronic nerve pain

A study from The University of Texas MD Anderson Cancer Center suggests that cancer drugs may hold promise in treating chronic nerve pain. Researchers found that BRAF, a protein linked to cancer, plays a crucial role in developing, amplifying, and sustaining chronic pain resulting from nerve damage. Preclinical models indicated that BRAF inhibitors reduced pain sensitivity, indicating potential therapeutic benefits for chronic nerve pain treatment.

The study, co-led by Shao-Rui Chen and Hui-Lin Pan, reveals that BRAF moves from peripheral sensory nerves to spinal cord terminals after injury, activating molecular signals that boost NMDA receptor activity. This heightened NMDA receptor activity amplifies pain signals. In preclinical trials, the BRAF inhibitor vemurafenib and MEK inhibitor selumetinib reduced sensitivity to touch, pressure, and heat.

Deleting the Braf gene also led to less persistent pain sensitivity. Nonetheless, these findings are preliminary, and researchers must investigate appropriate dosing, delivery methods, and potential side effects before clinical trials in humans. The team also aims to understand how nerve injury causes BRAF to move from nerves to the spinal cord.

While further research is needed, these results suggest that BRAF signaling may be connected to NMDA receptor activation in the spinal cord and that existing BRAF inhibitors could be repurposed to treat neuropathic pain.