Paper

Prostate Cancer and Prostatic Diseases (2004) 7, 105–110. doi:10.1038/sj.pcan.4500716

Whole-mount prostate sections reveal differential endoglin expression in stromal, epithelial, and endothelial cells with the development of prostate cancer

Presented at the American Urology Association Meeting, 24–29 May, no 566, 2002. Orlando, FL, USA

W Kassouf1, H R A Ismail1,2, A G Aprikian1 and S Chevalier1

1Urologic Oncology Research Group, Research Institute, and Departments of Surgery, Urology Division, Medicine and Oncology, McGill University Health Center, Montreal, Canada

Correspondence: S Chevalier, Research Institute, McGill University Health Center, 1650 Cedar Avenue, Montreal, QC, Canada H3G 1A4. E-mail: simone.chevalier@mcgill.ca

2Equal first author.

Received 15 September 2003; Revised 30 January 2004; Accepted 11 February 2004.

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Abstract

Endoglin is a nonsignaling receptor for transforming growth factor that contributes to the action of this growth factor in diverse cell types. It may also exhibit a function of its own. Endoglin levels vary with disease states and is a marker of new blood vessels. We studied endoglin expression in whole-mount prostate sections from 64 patients with localized prostate cancer, assessing reactivity in the epithelium, the stroma, and blood vessels. Cells in normal/benign acini were negative but significantly immunoreactive (P<0.001) in both prostatic intraepithelial neoplasia (PIN; 52% of cases) and malignant areas (77% of cases). In tumors, this involved less than 25% of malignant cells in 59% of specimens. The endoglin-stained stroma was detected mainly in areas surrounding PIN acini and tumors. Endoglin antibodies detected more microvessels than von Willebrand Factor antibodies in all prostatic areas (P<0.01). In addition, the number of microvessels increased with the development of cancer and correlated with Gleason score (P<0.01). Changes in endoglin expression in PIN and malignant cells, the surrounding stroma, and related blood vessels, suggest that endoglin function may be altered in prostate cancer.

Keywords:

prostatic stroma, prostatic epithelium, angiogenesis, endoglin, transforming growth factor-beta

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