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The Epidermal Growth Factor Receptor: A Role in Repair of Radiation-Induced DNA Damage

Authors' Affiliation: Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas

Requests for reprints: Chaitanya Nirodi, Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, 2201 Inwood Road, NC2.14C, Dallas, TX 75390-9187.

Abstract

The epidermal growth factor receptor (EGFR), which is frequently expressed in tumors of epithelial origin, is an important determinant of tumor responses to ionizing radiation. Elevated EGFR expression and activity frequently correlate with tumor resistance to radiotherapy in patients. EGFR is thought to confer tumor resistance to radiation through the activation of survival and cell proliferation pathways. Recent discoveries have identified a novel radioprotective function of EGFR which involves the radiation-induced nuclear translocation of the receptor and its interactions with the DNA-dependent protein kinase, a key component of the nonhomologous end-joining DNA repair pathway. Targeting the DNA repair function of EGFR may serve as a therapeutic model for sensitizing tumors to radiotherapy in patients.