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First published online on January 23, 2008
This version published online on March 28, 2008
Endocrine Reviews, doi:10.1210/er.2006-0045
A more recent version of this article appeared on April 1, 2008
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Crosstalk between the Estrogen Receptor and the HER Tyrosine Kinase Receptor Family: Molecular Mechanism and Clinical Implications for Endocrine Therapy Resistance

Grazia Arpino, Lisa Wiechmann, C. Kent Osborne, and Rachel Schiff*

Lester and Sue Smith Breast Center (L.W., C.K.O., R.S.), and the Dan L. Duncan Cancer Center (G.A., L.W., C.K.O., R.S.), the Department of Medicine (G.A., L.W., C.K.O., R.S.), and the Department of Molecular and Cellular Biology (C.K.O., R.S.), Baylor College of Medicine, Houston, Texas 77030

* To whom correspondence should be addressed. E-mail: rschiff{at}bcm.tmc.edu.

Breast cancer evolution and tumor progression are governed by the complex interactions between steroid receptor [estrogen receptor (ER) and progesterone receptor] and growth factor receptor signaling. In recent years, the field of cancer therapy has witnessed the emergence of multiple strategies targeting these specific cancer pathways and key molecules (ER and growth factor receptors) to arrest tumor growth and achieve tumor eradication; treatment success, however, has varied and both de novo (up front) and acquired resistance have proven a challenge. Recent studies of ER biology have revealed new insights into ER action in breast cancer and have highlighted the role of an intimate crosstalk between the ER and HER family signaling pathways as a fundamental contributor to the development of resistance to endocrine therapies against the ER pathway. The aim of this review article is to summarize the current knowledge on mechanisms of resistance of breast cancer cells to endocrine therapies due to the crosstalk between the ER and the HER growth factor receptor signaling pathways and to explore new available therapeutic strategies that could prolong duration of response and circumvent endocrine resistant tumor growth.







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