Crosstalk between the epidermal growth factor receptor and androgen receptor signaling pathways in prostate cancer. doi: http://dx.doi.org/10.5016/1806-8774.2009v11pT102

Authors

  • Christopher W. Gregory Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill and Clinsys Clinical Research, Inc.

DOI:

https://doi.org/10.5016/1806-8774.2009v11pT102

Abstract

Malignant cells are characterized by complex and often overlapping signaling pathways that modulate uncontrolled proliferation, leading to tumor growth and cancer progression. Prostate cancer is characterized by a dependence on androgens for growth initiation, and androgen deprivation is the standard treatment for advanced disease. Invariably, progression to castration-resistant prostate cancer (CRPC) occurs. Effective treatment options are currently limited to cytotoxic chemotherapy. In addition to androgen-mediated androgen receptor (AR) signaling in CRPC, multiple growth factor pathways are active, including the epidermal growth factor (EGF) receptor family of tyrosine kinases. Crosstalk between these two pathways has been studied in prostate cancer cell lines, xenograft tumor models, and in prostate cancer patients. This manuscript will focus on EGFR signaling, AR signaling, EGFR-AR crosstalk, and therapies targeted at these receptor-mediated regulatory pathways in CRPC.

Author Biography

Christopher W. Gregory, Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill and Clinsys Clinical Research, Inc.

Clinsys Clinical Research, Inc., 8540 Colonnade Center Drive, Suite 501, Raleigh NC 27615 and Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, CB# 7525, Chapel Hill NC 27599.

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Published

2010-02-21

Issue

Vol. 11 (2009)

Section

Theme Topic on "Cell Receptors and Signaling"

License

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