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Biology of Interactions: Antiepidermal Growth Factor Receptor Agents

Paul M. Harari, Gregory W. Allen, James A. Bonner

From the Department of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, WI; and the Department of Radiation Oncology, University of Alabama School of Medicine, Birmingham, AL

Address reprint requests to Paul M. Harari, MD, Department of Human Oncology, University of Wisconsin School of Medicine and Public Health, 600 Highland Ave, K4/336, Madison, WI 53792; e-mail: harari{at}humonc.wisc.edu

Epidermal growth factor receptor (EGFR) signaling inhibition represents a highly promising arena for the application of molecularly targeted cancer therapies. Evolving from several decades of systematic research in cancer cell biology, a series of EGFR inhibitors from both the monoclonal antibody (mAb) and tyrosine kinase inhibitor (TKI) class have been developed and promoted into clinical application. Several EGFR inhibitors have recently gained US Food and Drug Administration approval for cancer therapy in the United States (and many other countries), including the mAbs cetuximab and panitumumab, and the small molecule TKIs gefitinib, erlotinib, and lapatinib. The rapidly expanding preclinical and clinical data contributing to these US Food and Drug Administration drug registrations validates a central role of the EGFR as an important molecular target in epithelial malignancies. In this review, we focus primarily on the biology of EGFR interactions. Through improved understanding of EGFR biology in human cancers, there is anticipation that more tumor-selective therapy approaches with diminished collateral normal tissue toxicity can be advanced. Many questions remain to be answered, particularly with regard to how best combine EGFR inhibitors with conventional cancer therapies, and how to select those patients (tumors) most likely to benefit from EGFR inhibition strategies.

Authors' disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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