1. ¹Department of Pathology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
2. ²Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
3. ³Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
4. ⁴Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
5. ⁵Department of Pathology, Roswell Park Cancer Institute, Buffalo, NY, USA
6. ⁶Christiana Care Hospital, Department of Pathology, Wilmington, DE, USA
7. ⁷Department of Molecular and Biomedical Pharmacology, University of Kentucky, Lexington, KY, USA
8. ⁸Department of Surgery, University of Florida, Gainesville, FL, USA
9. ⁹Department of Biochemistry, University of Florida, Gainesville, FL, USA

Correspondence: Dr W Cance, MD, Health Science Center, PO Box 100286, 1600 SW Archer Road, Gainesville, FL 32610-0286, USA. E-mail: cance@surgery.ufl.edu

Received 7 January 2005; Revised 9 March 2005; Accepted 9 March 2005; Published online 29 April 2005.

Abstract

Focal adhesion kinase (FAK) is a protein tyrosine kinase expressed in invasive breast cancer that regulates antiapoptotic signaling. We have examined FAK expression by immunohistochemistry using anti-FAK 4.47 in breast tumor samples from a large population-based, case–control study of women participating in the University of North Carolina Breast Specialized Programs of Research Excellence (SPORE), Carolina Breast Cancer Study. In this population, 629 formalin-fixed, paraffin-embedded tissue sections were stained for FAK and scored as high (3+ or 4+ intensity and 90% positive cells) or otherwise. High FAK expression was associated with poor prognostic indicators including high mitotic index (>10 mitoses per 10 consecutive high-power fields), nuclear grade 3, architectural grade 3, estrogen and progesterone receptor negative, and HER-2/neu overexpressed using CB11 antibody. The association of high FAK expression with HER-2/neu overexpression lends further support that HER-2/neu and FAK collaborate to promote tumorigenesis. The presence of strong FAK expression in many high grade, estrogen- and progesterone-negative breast carcinomas indicates that FAK may be an attractive target for therapeutic intervention.