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JNCI Journal of the National Cancer Institute 2003 95(24):1813-1815; doi:10.1093/jnci/djg134
© 2003 by Oxford University Press
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© 2003 Oxford University Press

EDITORIAL

Is There a Role for Epidermal Growth Factor Receptor Inhibitors in Breast Cancer Prevention?

Gottfried E. Konecny, Cindy A. Wilson, Dennis J. Slamon

Affiliation of authors: David Geffen School of Medicine, University of California at Los Angeles.

Correspondence to: Dennis J. Slamon, MD, PhD, Peter Ueberroth Bldg. 3360B, 10945 Le Conte Ave., University of California, Los Angeles, CA 90095-7077 (e-mail: dslamon@mednet.ucla.edu)

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Growth and differentiation of both normal and malignant human breast cancer cells are known to be regulated by steroid hormone and peptide growth factor receptors. Among the peptide growth factor receptors frequently implicated in breast cancer are members of the type I receptor tyrosine kinase family, which includes HER1 (epidermal growth factor receptor [EGFR]), HER2 (c-erbB-2), HER3, and HER4. Hetero- and homo-oligomerization of these growth factor receptors results in tyrosine kinase activation, receptor phosphorylation, and subsequent activation of substrates involved in cellular signal transduction. In experimental models (1–3) and clinical correlative studies (4–7), it has been shown that the peptide growth factor receptor and steroid hormone receptor pathways are closely linked to one another. Growth factor receptor activation can result in direct phosphorylation and activation of the estrogen receptor (ER) in an estrogen-independent manner and lead to a ligand-independent reduced expression . . . [Full Text of this Article]


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