Activation of the phosphatidylinositol 3-kinase (PI3K)-AKT pathway, regulates many normal cellular processes which include cell proliferation, survival, and motility. For these same reasons, the PI3K pathway also plays an important oncogenic role in many cancer types. PI3K signaling pathways can be deregulated by a variety of mechanisms in human tumors.

The Epidermal Growth Factor Receptor (EGFR) activates an important pathway that leads to cell proliferation, differentiation, migration/motility, adhesion, protection from apoptosis, enhanced survival and gene transcription.

V-raf murine sarcoma viral oncogene homolog B1, also known as BRAF, is a protein which in humans is encoded by the BRAF gene. The BRAF gene makes a protein called B-RAF, which is involved in sending signals in cells and in cell growth. This gene may be mutated (changed) in many types of cancer, which causes a change in the B-RAF protein. This can increase the growth and spread of cancer cells.

V-raf murine sarcoma viral oncogene homolog B1, also known as BRAF, is a protein which in humans is encoded by the BRAF gene. The BRAF gene makes a protein called B-RAF, which is involved in sending signals in cells and in cell growth. This gene may be mutated (changed) in many types of cancer, which causes a change in the B-RAF protein. This can increase the growth and spread of cancer cells.

The presence of the V600E mutation in the BRAF gene is associated with poor prognosis and non response to anti-EGFR therapy in advanced stage colorectal cancer patients. Studies show that colorectal cancer patients with wild-type KRAS failed to respond when treated with either cetuximab or panitumumab and experienced a shorter progression-free survival and overall survival, when the BRAF mutation was present, compared to patients with wild-type BRAF tumors.1