In a recent study, patients with mutated BRAF did not respond to treatment with two drugs that block epidermal growth factor receptors (EGFR) — Erbitux® (cetuximab) and Vectibix™ (panitumumab). Patients in the study all had normal, wild-type KRAS, another mutation that blocks response to Erbitux and Vectibix.
Proteins controlled by the BRAF gene lie in a pathway of signals between the cell surface and its nucleus and control cell division. When BRAF is mutated, uncontrolled cell growth can lead to cancer. Because a mutated gene is already active downstream of the receptor, trying to block the pathway by blocking an EGF receptor on the cell surface doesn’t work to control the cancer.
About 12 percent of patients with normal, wild-type KRAS had mutated BRAF in the study adding to the number of patients who did not respond to Erbitux or Vectibix.
Like KRAS, BRAF is a predictive biomarker that can help patients and doctors choose the best treatment for advanced colorectal cancer.