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Annals of Oncology Advance Access published online on January 15, 2009
Annals of Oncology, doi:10.1093/annonc/mdn710
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© The Author 2009. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Epidermal growth factor receptor as a potential therapeutic target in triple-negative breast cancer

B. Corkery1,2, J. Crown1,2, M. Clynes1 and N. O'Donovan1,*

1 National Institute for Cellular Biotechnology, Dublin City University
2 Department of Medical Oncology, St Vincent's University Hospital, Ireland

* Correspondence to: Dr N. O'Donovan, National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. Tel: +353-1-700-7497; Fax: +353-1-700-5484; E-mail: norma.odonovan{at}dcu.ie

Background: No proven targeted therapy is currently available for the treatment of triple-negative breast cancer (TNBC). Epidermal growth factor receptor (EGFR) is frequently overexpressed in TNBC. We studied the activity of EGFR antagonists alone, and in combination with chemotherapy, in TNBC cell lines.

Materials and methods: EGFR and phosphorylated EGFR were measured by enzyme-linked immunosorbent assay. Sensitivity to EGFR inhibitors alone and in combination with chemotherapy was assessed. Effects of gefitinib on EGFR signalling and cell cycle were also examined.

Results: EGFR was overexpressed in the TNBC compared with the human epidermal growth factor receptor 2 (HER-2)-positive cell lines. Phosphorylation of EGFR was detected in the TNBC cells in response to epidermal growth factor stimulation and was blocked by gefitinib treatment. However, the TNBC cell lines were less sensitive to EGFR inhibition than the HER-2-positive cell lines. Response to gefitinib was associated with reduced phosphorylation of both mitogen activated protein kinase (MAPK) and Akt and induction of G1 arrest. Gefitinib enhanced response to both carboplatin and docetaxel in the TNBC cells, and the triple combination of gefitinib, carboplatin and docetaxel was synergistic.

Conclusions: Although the TNBC cells are less sensitive to EGFR inhibition than the HER-2-positive cell lines, gefitinib enhanced response to chemotherapy. Gefitinib combined with carboplatin and docetaxel warrants further investigation in TNBC.

basal-like breast cancer, carboplatin, docetaxel, EGFR, gefitinib, triple-negative breast cancer

Received for publication April 22, 2008. Revision received October 18, 2008. Accepted for publication October 20, 2008.


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