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[Cancer Research 61, 1919-1926, March 1, 2001]
© 2001 American Association for Cancer Research


Endocrinology

Evaluation of Androgen, Estrogen (ER{alpha} and ERß), and Progesterone Receptor Expression in Human Prostate Cancer by Real-Time Quantitative Reverse Transcription-Polymerase Chain Reaction Assays

Alain Latil1, Ivan Bièche, Dominique Vidaud, Rosette Lidereau, Philippe Berthon, Olivier Cussenot and Michel Vidaud

CeRePP, Université Paris VII, F-91000 Evry [A. L., P. B., O. C.]; Laboratoire de Génétique Moléculaire, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, F-75006 Paris [I. B., D. V., M. V.]; Département d’Urologie, Université Paris VII, Hôpital Saint-Louis, F-75010 Paris [O. C.]; Institut Universitaire de France, F-75005 Paris [O. C.]; and Laboratoire d’Oncogénétique, Centre René Huguenin, F-92210 St. Cloud [I. B., R. L.], France

Steroid hormones can have profound effects on prostate tumor development making it important to define steroid receptor expression in prostate tissues. For this purpose, androgen receptor (AR) and estrogen receptor (ER{alpha} and ERß) expression was quantified in 12 clinically localized and 11 hormone-refractory sporadic prostate tumors, using real-time quantitative reverse transcription-PCR assays. To gain more insight into hormone-responsiveness, estrogen-regulated progesterone receptor (PGR) and androgen-regulated prostatic acid phosphatase (PAP) mRNA levels were also quantified. There is a decrease in expression of ERß in both clinically localized and hormone-refractory tumors relative to normal prostate tissues. Moreover, hormone-refractory tumors display a decreased expression of ER{alpha} and an increased expression of AR. There is a positive association between ER{alpha}, ERß, and PGR expression (P < 0.0001) and a negative association between AR and the androgen-regulated gene PAP expression in hormone-refractory tumors. Taken together, these data indicate that, although increased expression of the AR gene might play a key role in endocrine treatment failure, it cannot be considered as the sole actor of this unresolved dilemma, and abnormalities in ER{alpha} and/or ERß expression may also modulate the growth response of prostate cancer to hormone withdrawal. Our results also suggest that ER{alpha} and ERß expression status could be used to identify advanced prostate tumor patients who may respond to antiestrogen therapy.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2001 by the American Association for Cancer Research.