title: Postoperative prostate-specific antigen velocity independently predicts for failure of salvage radiotherapy after prostatectomy.
abstract: OBJECTIVE
  Identification of patients most likely to benefit from salvage radiotherapy (RT) using postoperative (postop) prostate-specific antigen (PSA) kinetics.
  
  
  METHODS
  From 1984 to 2004, 81 patients who fit the following criteria formed the study population: undetectable PSA after radical prostatectomy (RP); pathologically negative nodes; biochemical relapse defined as a persistently detectable PSA; salvage RT; and two or more postop PSAs available before salvage RT. Salvage RT included the whole pelvic nodes in 55 patients and 4 months of total androgen suppression in 56 patients. The median follow-up was >5 years. All relapses were defined as a persistently detectable PSA. Kaplan-Meier and Cox proportional hazards multivariable analysis were performed for all clinical, pathological, and treatment factors predicting for biochemical relapse-free survival (bRFS).
  
  
  RESULTS
  There were 37 biochemical relapses observed after salvage RT. The 5-year bRFS after salvage RT for patients with postop prostate-specific antigen velocity < or = 1 vs. >1 ng/ml/yr was 59% vs. 29%, p = 0.002. In multivariate analysis, only postop PSAV (p = 0.0036), pre-RT PSA level < or = 1 (p = 0.037) and interval-to-relapse >10 months (p = 0.012) remained significant, whereas pelvic RT, hormone therapy, and RT dose showed a trend (p = approximately 0.06). PSAV, but not prostate-specific antigen doubling time, predicted successful salvage RT, suggesting an association of zero-order kinetics with locally recurrent disease.
  
  
  CONCLUSIONS
  Postoperative PSA velocity independently predicts for the failure of salvage RT and can be considered in addition to high-risk features when selecting patients in need of systemic therapy following biochemical failure after RP. For well-selected patients, salvage RT can achieve high cure rates.
authors.affiliation: Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA. crking@stanford.edu
authors.forename: Christopher R
authors.initials: CR
authors.lastname: King
authors.forename: Joseph C
authors.initials: JC
authors.lastname: Presti
authors.forename: James D
authors.initials: JD
authors.lastname: Brooks
authors.forename: Harcharan
authors.initials: H
authors.lastname: Gill
authors.forename: Michael T
authors.initials: MT
authors.lastname: Spiotto
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000726:Androgen Antagonists / Q000627:therapeutic use; D018572:Disease-Free Survival; D006801:Humans; D008297:Male; D008875:Middle Aged; D018579:Patient Selection; D011184:Postoperative Period; D017430:Prostate-Specific Antigen / Q000097:blood*; D011468:Prostatectomy; D011471:Prostatic Neoplasms / Q000097:blood* / Q000188:drug therapy / Q000532:radiotherapy* / Q000601:surgery; D016879:Salvage Therapy / Q000379:methods*; D017211:Treatment Failure
chemical_list: D000726:Androgen Antagonists; D017430:Prostate-Specific Antigen