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Elevated levels of HER‐2/ neu and androgen receptor in clinically localized prostate cancer identifies metastatic potential
Author(s) -
Ricciardelli Carmela,
Jackson Michael W.,
Choong Catherine S.,
Stahl Jürgen,
Marshall Villis R.,
Horsfall David J.,
Tilley Wayne D.
Publication year - 2008
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.20747
Subject(s) - prostate cancer , androgen receptor , medicine , prostate , androgen , prostate disease , oncology , pathology , endocrinology , cancer research , cancer , hormone
BACKGROUND In this study, we investigated the expression of HER‐2/ neu and AR in clinically organ‐confined prostate cancer to determine whether alterations in these signaling pathways contribute to the development of metastatic disease. METHODS HER‐2/ neu and AR immunoreactivity were evaluated in archived prostatic tissues obtained from 53 men with clinically organ‐confined disease who underwent radical prostatectomy. Associations between AR and HER‐2/ neu immunostaining and disease outcome were determined. RESULTS Seventy percent (37/53) of tumors exhibited high levels of HER‐2/ neu immunostaining and 68% (36/53) of tumors had elevated AR levels. Patients with high levels of both HER‐2/ neu and AR had the highest rate of PSA failure (56%, 15/27) compared with no PSA failures amongst seven patients with low levels of both HER‐2/ neu and AR (log rank statistic 7.69, P = 0.021). Concurrent high levels of HER‐2/ neu and AR expression were significantly associated with high pathological stage ( P = 0.027) and development of metastatic disease ( P = 0.022). CONCLUSIONS These findings support the notion that both the HER‐2/ neu and AR signaling pathways may contribute to development of metastatic disease. The subset of prostate tumors with increased HER‐2/ neu and AR levels may benefit from treatment strategies that target both signaling pathways. Prostate 68:830–838, 2008. © 2008 Wiley‐Liss, Inc.