Overcoming resistance to BRAFV600E inhibition in melanoma by deciphering and targeting personalized protein network alterations

BRAF V600E melanoma patients, despite initially responding to the clinically prescribed anti-BRAF V600E therapy, often relapse, and their tumors develop drug resistance. While it is widely accepted that these tumors are originally driven by the BRAF V600E mutation, they often eventually diverge and become supported by various signaling networks. Therefore, patient-specific altered signaling signatures should be deciphered and treated...