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[Cancer Research 57, 3189-3193, August 1, 1997]
© 1997 American Association for Cancer Research

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Aberrant E-Cadherin and {alpha}-Catenin Expression in Prostate Cancer: Correlation with Patient Survival1

Paul J. M. Richmond, Anastasios J. Karayiannakis, Akira Nagafuchi, Amir V. Kaisary and Massimo Pignatelli2

Department of Surgery, Royal Free Hospital, London NW3 2QC, United Kingdom [P. J. M. R., A. V. K.]; Department of Surgery [A. J. K.] and Cell Adhesion Laboratory. Department of Histopathology [M. P.], Royal Postgraduate Medical School, Du Cane Road, London W12 0NN, United Kingdom; and Department of Cell Biology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan [A. N.]

E-cadherin maintains the normal differentiated phenotype in epithelial cells; this function is partly mediated by {alpha}-catenin, which links E-cadherin to the cell cytoskeleton. Dysfunction of E-cadherin in vitro and in vivo is associated with an invasive phenotype. However, the role of {alpha}-catenin is largely undetermined. We analyzed the expression of E-cadherin and {alpha}-catenin in prostate cancer to assess the relationship of abnormal expression to stage, grade and survival. E-cadherin expression was evaluated in 99 prostate cancers. In 79 of those specimens, {alpha}-catenin was also assessed. In benign prostatic epithelium, both E-cadherin and {alpha}-catenin were expressed uniformly at the cell membrane. Abnormal E-cadherin expression was found in 56% of cancer specimens, whereas {alpha}-catenin expression was abnormal in 42%. Abnormal expression of each molecule was significantly correlated with Gleason score (P < 0.0001) and the ratio of resection chippings infiltrated by tumor (P < 0.0001). E-cadherin expression was also associated with the extent of disease on the initial bone scan (P = 0.017). Univariate analysis showed significantly lower survival rate for patients with abnormal E-cadherin (P = 0.0003) or {alpha}-catenin expression (P = 0.031). Multivariate regression analysis showed that the prognostic value of E-cadherin was independent of tumor grade but not of metastasis. These results suggest that perturbation of cell-cell adhesion is involved in the progression of prostate cancer and that analysis of E-cadherin expression may be clinically useful.

1 A. J. K. was supported by a scholarship in Surgical Oncology from the Greek State Scholarships Foundation.

2 To whom requests for reprints should be addressed. Phone: 44-181-383-2432; Fax: 44-181-740-7417; E-mail: m.pignatelli@rpms.ac.uk.

Received 1/23/97. Accepted 5/29/97.




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Copyright © 1997 by the American Association for Cancer Research.