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Androgen receptor levels in prostate cancer epithelial and peritumoral stromal cells identify non‐organ confined disease
Author(s) -
Ricciardelli Carmela,
Choong Catherine S.,
Buchanan Grant,
Vivekanandan Suchindra,
Neufing Petra,
Stahl Jürgen,
Marshall Villis R.,
Horsfall David J.,
Tilley Wayne D.
Publication year - 2005
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20154
Subject(s) - stromal cell , prostate cancer , androgen receptor , prostatectomy , medicine , prostate , stroma , pathology , immunostaining , cancer , oncology , urology , immunohistochemistry
Abstract BACKGROUND Although up to 30% of men who undergo radical prostatectomy for clinically organ‐confined prostate cancer will relapse with disseminated disease, currently it is not possible to predict these patients. METHODS Androgen receptor (AR) immunoreactivity in stromal and epithelial compartments of tumor foci was evaluated by video image analysis in 53 radical prostatectomy specimens. Kaplan–Meier and Cox Regression analyses were used to determine whether AR immunostaining was related to rate and risk of relapse, respectively. RESULTS Ninety‐eight percent (52/53) of the tumors contained AR positive malignant epithelial cells. Kaplan–Meier analysis indicated that patients with high AR levels (>64% AR positive nuclear area) in the malignant epithelial cells or low AR levels (≤45% AR positive nuclear area) in the peritumoral stroma cells, were more likely to relapse earlier following radical prostatectomy. The shortest time to relapse and the highest relapse rate was for patients with both high AR in the malignant epithelial cells and low AR in the peritumoral stromal cells. CONCLUSIONS These findings suggest that AR is an important determinant of disease relapse in early stage prostate cancer, and that altered AR levels in the malignant epithelial cells or in the peritumoral stroma is indicative of non‐organ confined prostate cancer. © 2004 Wiley‐Liss, Inc.