Philadelphia, PA 19111, USA Full list of author information is available at the end of the articleFor many solid tumors, overexpression or activating mu-tation of the epidermal growth factor receptor (EGFR) serves as an oncogenic driver. Even in some tumors in which EGFR is not overexpressed, it can serve as an essen-tial intermediate in signaling required for cell growth and survival [1, 2], reflecting its role as a potent regulator of multiple downstream effector cascades, including PI3K/ AKT/mTOR, JAK/STAT, and RAS/RAF/MEK. Because of EGFR have been developed. These include monoclonal antibodies such as cetuximab and panitumumab, which target the extracellular domain, and small molecule inhibi-tors including erlotinib, gefitinib, lapatinib, and afatinib, which target the cytosolic kinase domain. These agents often provide significant clinical benefit, but are some-times ineffective because of intrinsic or acquired tumor resistance factors. Mechanisms of resistance can include expression of an EGFRvIII variant , which eliminates the epitope for some monoclonal antibodies, or missense mutations involving the EGFR kinase domain (e.g.
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