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Japanese Journal of Clinical Oncology Advance Access originally published online on August 12, 2008
Japanese Journal of Clinical Oncology 2008 38(9):617-622; doi:10.1093/jjco/hyn071
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© The Author (2008). Published by Oxford University Press. All rights reserved

Undetectable Level of Prostate Specific Antigen (PSA) Nadir Predicts PSA Biochemical Failure in Local Prostate Cancer with Delayed-combined Androgen Blockade

Norihito Soga, Kiminobu Arima and Yoshiki Sugimura

Division of Nephro-Urologic Surgery and Andrology, Department of Reparative and Regenerative Medicine, Institute of Medical Life Science, Mie University Graduate School of Medicine, Tsu, Mie, Japan

For reprints and all correspondence: Norihito Soga, Division of Nephro-Urologic Surgery and Andrology, Department of Reparative and Regenerative Medicine, Institute of Medical Life Science, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. E-mail: n-soga{at}clin.medic.mie-u.ac.jp

Received June 8, 2008; accepted July 14, 2008

Objective: To determine optimal predictors with which to select the crucial patients enrolled in delayed-combined androgen blockade (CAB) trials, based on risk factors.

Methods: From January 2001 to December 2004, 92 prostate cancer patients with T1c, T2 and T3aN0M0 were enrolled in a clinical trial. Medical castration and anti-androgen treatment were used sequentially as delayed-CAB. The prostate specific antigen (PSA) nadir was determined following medical castration only. Anti-androgen treatment was administered if a PSA progression was observed and the subsequent PSA response was evaluated. Time to PSA biochemical failure, induced by medical castration or with anti-androgen treatment, was estimated. Risk factors of PSA failure were evaluated by multivariate analysis.

Results: During luteinizing hormone–releasing hormone (LH–RH) monotherapy, a Kaplan–Meier analysis estimated that the proportion of patients without PSA progression was 64.8% at 5 years. In the multivariate analysis of the prediction of PSA progression with LH–RH monotherapy, a Gleason score over 8, initial PSA >20 ng/ml and PSA nadir >0.2 ng/ml were significant independent risk factors that affected PSA biochemical failure. The PSA progression-free rate in the lower PSA nadir group was significantly lower than that in the other. The 25 patients in the higher PSA nadir group were treated with anti-androgen therapy. Under anti-androgen therapy, the PSA progression-free rate was 62.6% at 5 years. Only PSA nadir >0.2 ng/ml was a significant independent risk factor. The PSA progression-free rate in the lower PSA nadir group was significantly lower than the other.

Conclusions: PSA nadir was the optimal predictive for low stage, non-metastatic population during delayed-CAB.

Key Words: nadir PSA • PSA biochemical failure • delayed-CAB


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