title: Undetectable level of prostate specific antigen (PSA) nadir predicts PSA biochemical failure in local prostate cancer with delayed-combined androgen blockade.
abstract: 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.
authors.affiliation: 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. n-soga@clin.medic.mie-u.ac.jp
authors.forename: Norihito
authors.initials: N
authors.lastname: Soga
authors.forename: Kiminobu
authors.initials: K
authors.lastname: Arima
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Sugimura
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000726:Androgen Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D000813:Anilides / Q000008:administration & dosage / Q000494:pharmacology; D018931:Antineoplastic Agents, Hormonal / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000494:pharmacology* / Q000627:therapeutic use; D004334:Drug Administration Schedule; D016903:Drug Monitoring; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D017273:Goserelin / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D053208:Kaplan-Meier Estimate; D016729:Leuprolide / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009570:Nitriles / Q000008:administration & dosage / Q000494:pharmacology; D018579:Patient Selection; D016016:Proportional Hazards Models; D017430:Prostate-Specific Antigen / Q000097:blood / Q000187:drug effects*; D011471:Prostatic Neoplasms / Q000188:drug therapy*; D012307:Risk Factors; D014105:Tosyl Compounds / Q000008:administration & dosage / Q000494:pharmacology; D017211:Treatment Failure
chemical_list: D000726:Androgen Antagonists; D000813:Anilides; D018931:Antineoplastic Agents, Hormonal; D009570:Nitriles; D014105:Tosyl Compounds; D017273:Goserelin; D007987:Gonadotropin-Releasing Hormone; C053541:bicalutamide; D017430:Prostate-Specific Antigen; D016729:Leuprolide