- Top of page
- KRAS mutations and sensitivity to therapy with mAb to epidermal growth factor receptor in colorectal cancer
- KRAS mutation as a mechanism of resistance to EGFR-targeted therapy
- EGFR mutations and sensitivity to EGFR-tyrosine kinase inhibitor therapy in non–small cell lung cancer
- EGFR mutation as a mechanism underlying sensitivity to therapy with EGFR-TKIs
- Molecular mechanisms associated with acquired resistance to therapy with EGFR-TKIs
The discovery that signaling by the epidermal growth factor receptor (EGFR) plays a key role in tumorigenesis prompted efforts to target this receptor in anticancer therapy. Two different types of EGFR-targeted therapeutic agents were subsequently developed: mAbs, such as cetuximab and panitumumab, which target the extracellular domain of the receptor, thereby inhibiting ligand-dependent EGFR signal transduction; and small-molecule tyrosine kinase inhibitors, such as gefitinib and erlotinib, which target the intracellular tyrosine kinase domain of the EGFR. Furthermore, recent clinical and laboratory studies have identified molecular markers that have the potential to improve the clinical effectiveness of EGFR-targeted therapies. This minireview summarizes the emerging role of molecular profiling in guiding the clinical use of anti-EGFR therapeutic agents.