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Journal of Biomedicine and Biotechnology
Volume 2007, Article ID 97939, 4 pages
Research Article

EGFR Activation and Ultraviolet Light‐Induced Skin Carcinogenesis

1Cancer Center, Creighton University Medical Center, Omaha 68178, NE, USA
2Department of Biomedical Sciences, School of Medicine, Creighton University, 2500 California Plaza, Omaha 68178, NE, USA

Received 15 December 2006; Accepted 14 February 2007

Academic Editor: Honnavara N. Ananthaswamy

Copyright © 2007 Taghrid B. El-Abaseri and Laura A. Hansen. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The epidermal growth factor receptor (EGFR) regulates the proliferation of keratinocytes through multiple mechanisms that differ depending on the localization of the cell within the skin. Ultraviolet (UV) irradiation, the main etiologic factor in the development of skin cancer, also activates the receptor. In this review, we discuss how the UV-induced activation of EGFR regulates the response of the skin to UV. UV-induced EGFR activation increases keratinocyte proliferation, suppresses apoptosis, and augments and accelerates epidermal hyperplasia in response to UV. Pharmacological inhibition of the UV-induced activation of EGFR in a genetically initiated mouse skin tumorigenesis model suppresses tumorigenesis and the activation of mitogen-activated protein (MAP) kinases and phosphatidyl inositol-3-kinase (PI3K)/AKT signaling pathways. EGFR has pleiotropic, complex, and cell-type-specific functions in cutaneous keratinocytes; suggesting that the receptor is an appropriate target for the development of molecularly targeted therapies for skin cancer and other pathologies.