
Researchers at The University of Texas MD Anderson Cancer Centre discovered that the protein BRAF amplifies pain signals by increasing the activity of NMDA receptors after nerve injury.
Preclinical models showed that blocking BRAF signalling reduced pain sensitivity, suggesting that existing cancer drugs targeting this protein could eventually be repurposed for neuropathic pain treatment.
Co-led by Shao Rui Chen and Hui Lin Pan, the study published in Science Signaling emphasizes that clinical human trials are required to confirm safety and efficacy for pain management.