This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Genther Williams, S. M. Articles by Lambert, P. F. Search for Related Content PubMed PubMed Citation Articles by Genther Williams, S. M. Articles by Lambert, P. F.

Requirement of Epidermal Growth Factor Receptor for Hyperplasia Induced by E5, a High-Risk Human Papillomavirus Oncogene

¹ McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, Wisconsin; ² Department of Pathology, Georgetown University Medical School, Washington, District of Columbia; and ³ Department of Genetics and the Lineberger Cancer Center, University of North Carolina, Chapel Hill, North Carolina

Requests for reprints: Paul F. Lambert, McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1400 University Avenue, Madison, WI 53706. Phone: 608-262-8533; Fax: 608-262-2824; E-mail: lambert{at}oncology.wisc.edu.

Multicellular organisms rely on complex networks of signaling cascades for development, homeostasis, and responses to the environment. These networks involve diffusible signaling molecules, their receptors, and a variety of downstream effectors. Alterations in the expression or function of any one of these factors can contribute to disease, including cancer. Many viruses have been implicated in cancer, and some of these modulate cellular signal transduction cascades to carry out their life cycles. High-risk human papillomaviruses (HPVs), the causative agents of most cervical and anogenital cancers, encode three oncogenes. One of these, E5, has been postulated to transform cells in tissue culture by modulating growth factor receptors. In this study, we generate and characterize transgenic mice in which the E5 gene of the most common high-risk HPV, HPV16, is targeted to the basal layer of the stratified squamous epithelium. In these mice, E5 alters the growth and differentiation of stratified epithelia and induces epithelial tumors at a high frequency. Through the analysis of these mice, we show a requirement of the epidermal growth factor receptor for the hyperplastic properties of E5.

This article has been cited by other articles:

				J. A. Regan and L. A. Laimins Bap31 Is a Novel Target of the Human Papillomavirus E5 Protein J. Virol., October 15, 2008; 82(20): 10042 - 10051. [Abstract] [Full Text] [PDF]

				E. Krawczyk, F. A. Suprynowicz, X. Liu, Y. Dai, D. P. Hartmann, J. Hanover, and R. Schlegel Koilocytosis: A Cooperative Interaction between the Human Papillomavirus E5 and E6 Oncoproteins Am. J. Pathol., September 1, 2008; 173(3): 682 - 688. [Abstract] [Full Text] [PDF]

				J. P. Maufort, S. M. Genther Williams, H. C. Pitot, and P. F. Lambert Human Papillomavirus 16 E5 Oncogene Contributes to Two Stages of Skin Carcinogenesis Cancer Res., July 1, 2007; 67(13): 6106 - 6112. [Abstract] [Full Text] [PDF]

				M. Nonnenmacher, J. Salmon, Y. Jacob, G. Orth, and F. Breitburd Cottontail rabbit papillomavirus e8 protein is essential for wart formation and provides new insights into viral pathogenesis. J. Virol., May 1, 2006; 80(10): 4890 - 4900. [Abstract] [Full Text] [PDF]