Emergence of Multiple <i>EGFR</i> Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer

Abstract

Colorectal tumors evade EGFR blockade by constitutive activation of downstream signaling effectors and through mutations affecting receptor-antibody binding. Both mechanisms of resistance may occur concomitantly. Our data have implications for designing additional lines of therapy for patients with colorectal cancer who relapse upon treatment with anti-EGFR antibodies.