PMID- 15491740
OWN - NLM
STAT- MEDLINE
DCOM- 20050812
LR  - 20071114
IS  - 1527-9995 (Electronic)
IS  - 0090-4295 (Linking)
VI  - 64
IP  - 4
DP  - 2004 Oct
TI  - Metastases of prostate cancer express estrogen receptor-beta.
PG  - 814-20
AB  - OBJECTIVES: To examine estrogen receptor-beta (ERbeta) expression in prostate 
      cancer (CaP) metastases, thereby providing a basis for conducting estrogen 
      therapy studies in patients with metastatic CaP. Advanced androgen-independent 
      CaP is a serious health problem with no effective treatment at present. Estrogens 
      have been reported to inhibit the growth of CaP cells in androgen-free 
      environments. Recent reports have shown that the prostatic epithelium and primary 
      CaP cells express ERbeta, with decreased expression of ERbeta accompanying CaP 
      progression. It has been proposed that ERbeta may play a role in the growth 
      regulation of prostate cells. The targeting of ERs by selective ER modulators 
      might be an effective method of treating advanced CaP. METHODS: The anti-ERbeta 
      antibody GC17 was used in immunohistochemistry to characterize the expression of 
      ERbeta in CaP metastasis specimens (n = 60) obtained from 20 patients who had 
      died of CaP. Statistical analyses were performed to evaluate the association of 
      ERbeta expression with clinical parameters, including prostate-specific antigen 
      levels, radiotherapy, and estrogen exposure. RESULTS: Nuclear ERbeta staining was 
      detected in all bone CaP metastases (33 of 33) and nonosseous CaP metastases (27 
      of 27). However, a large variability in the percentage of immunoreactive cells 
      (5% to 100%) was found among patients, as well as among individual patient 
      samples. A statistically significant negative association between nuclear ERbeta 
      staining and estrogen exposure (P = 0.05) was detected. CONCLUSIONS: Our data 
      have shown that ERbeta is expressed in CaP metastases, validating the initiation 
      of studies to evaluate selective ER modulators for treatment of advanced CaP.
FAU - Lai, Janice S
AU  - Lai JS
AD  - Department of Urology, University of Washington School of Medicine, Seattle, 
      Washington 98195, USA.
FAU - Brown, Lisha G
AU  - Brown LG
FAU - True, Lawrence D
AU  - True LD
FAU - Hawley, Sarah J
AU  - Hawley SJ
FAU - Etzioni, Ruth B
AU  - Etzioni RB
FAU - Higano, Celestia S
AU  - Higano CS
FAU - Ho, Shuk-Mei
AU  - Ho SM
FAU - Vessella, Robert L
AU  - Vessella RL
FAU - Corey, Eva
AU  - Corey E
LA  - eng
GR  - 1 P50 CA97186-02/CA/NCI NIH HHS/United States
GR  - DK1084-01/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Urology
JT  - Urology
JID - 0366151
RN  - 0 (Antineoplastic Agents, Hormonal)
RN  - 0 (Estrogen Receptor beta)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Receptors, Androgen)
SB  - IM
MH  - Adenocarcinoma/*chemistry/*secondary
MH  - Aged
MH  - Antineoplastic Agents, Hormonal/therapeutic use
MH  - Bone Neoplasms/*chemistry/secondary
MH  - Cell Nucleus/chemistry
MH  - Estrogen Receptor beta/*analysis
MH  - Humans
MH  - Liver Neoplasms/chemistry/secondary
MH  - Lung Neoplasms/chemistry/secondary
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Proteins/*analysis
MH  - Neoplasms, Hormone-Dependent/*chemistry/*secondary
MH  - Prostatic Neoplasms/drug therapy/*pathology/radiotherapy
MH  - Receptors, Androgen/analysis
EDAT- 2004/10/20 09:00
MHDA- 2005/08/13 09:00
CRDT- 2004/10/20 09:00
PHST- 2004/03/25 00:00 [received]
PHST- 2004/05/25 00:00 [accepted]
PHST- 2004/10/20 09:00 [pubmed]
PHST- 2005/08/13 09:00 [medline]
PHST- 2004/10/20 09:00 [entrez]
AID - S0090-4295(04)00692-2 [pii]
AID - 10.1016/j.urology.2004.05.036 [doi]
PST - ppublish
SO  - Urology. 2004 Oct;64(4):814-20. doi: 10.1016/j.urology.2004.05.036.