1465 DOES SALVAGE RADIATION THERAPY CHANGE THE BIOLOGY OF RECURRENT PROSTATE CANCER BASED ON PSA DOUBLING TIMES? RESULTS FROM THE SEARCH DATABASE

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You have accessJournal of UrologyProstate Cancer: Localized VII1 Apr 20121465 DOES SALVAGE RADIATION THERAPY CHANGE THE BIOLOGY OF RECURRENT PROSTATE CANCER BASED ON PSA DOUBLING TIMES? RESULTS FROM THE SEARCH DATABASE Roberto Muller, Joseph Presti, William Aronson, Martha Terris, Christopher Kane, Christopher Amling, and Stephen Freedland Roberto MullerRoberto Muller Durham, NC More articles by this author , Joseph PrestiJoseph Presti Stanford and Palo Alto, CA More articles by this author , William AronsonWilliam Aronson Los Angeles and West Los Angeles, CA More articles by this author , Martha TerrisMartha Terris Augusta, GA More articles by this author , Christopher KaneChristopher Kane San Diego, CA More articles by this author , Christopher AmlingChristopher Amling Portland, OR More articles by this author , and Stephen FreedlandStephen Freedland Durham, NC More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2012.02.1986AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Salvage radiation therapy (SRT) offers a second opportunity for prostate cancer (PCa) control after biochemical recurrence (BCR) in men treated with radical prostatectomy (RP). Although some retrospective data suggest an overall survival benefit, we hypothesized that in men with radio-resistant tumors, SRT may indeed promote transformation to a more aggressive cancer due to radiation-induced mutations. To test this, we used PSA doubling time (PSADT) as a surrogate for cancer aggressiveness and compared PSADT before and after SRT in men who failed SRT. METHODS Of 287 men who underwent SRT in SEARCH database since 1988, we detected 78 with SRT failure defined as PSA ≥ 0.2 ng/mL above the post-SRT nadir. Of these, 44 had PSADT available before and after SRT, which was compared using Wilcoxon's paired test with men serving as their own controls. Correlation between PSADT pre- and post-SRT was also measured using a non-parametric test (Spearman's test). We tested predictors of PSADT change using multivariable logistic regression. RESULTS Baseline data are in Table 1. PSADT after BCR and after SRT were only weakly correlated (Spearman's rho=0.154; Fig. 1). There were no differences in PSADT before and after SRT (10.6 vs. 12.2 months; P=0.85; Table 2). However, in some individual cases large changes were observed. Only seminal vesicle invasion showed a trend towards an association with a shorter post-SRT PSADT relative to the pre-SRT PSADT (P=0.067). Table 1. Baseline Data of Patients that Failed SRT and have PSADT Available After BCR and SRT Failure Characteristic Final population (n=44) Age at surgery, yrs. Median (IQR) 62.5(59-65) Range 50-75 PSA before surgery, ng/mL Median (IQR) 10.6(7.0-27.2) Range 1.5-70.9 PSA before SRT, ng/mL Median (IQR) 1.1(0.6-1.9) Range 0.1-9.3 Pathological Gleason score, no. (%) 2-6 13(29.6) 7 21(47.7) 8-10 10(22.7) Extracapsular extension, no. (%) 19(43.2) Positive surgical margins, no. (%) 23(52.3) Seminal vesicle invasion, no. (%) 15(34.1) Positive lymph nodes, no. (%) 1(2.3) Persistent detectable PSA nadir after surgery⁎, no. (%) 26(59.1) Radiation dosage⁎⁎, cGy Median (IQR) 6600(6600-6660) Range 6120-7200 ⁎ Defined as PSA nadir within 6 months of surgery ≥0.03 ng/mL; ⁎⁎ dosage available only in 24 patients. Table 2. Comparison Between PSADT After BCR and SRT failure and Characteristics of the Pool of PSA Samples Used for PSADT Calculation After BCR (n=44) After SRT failure (n=44) P⁎ PSADT, months .85 Median (IQR) 10.6(6.7-24.5) 12.2(7.9-21.6) Range 2.4-100 1.5-100 Interval between consecutive samples, days .87 Median (IQR) 120.1(71.0-171.3) 123.3(90.5-171.8) Range 44.0-403.0 46.4-340.0 Number of samples .02 Mean (SD) 4.3(2.2) 5.3(2.5) Range 2-11 2-15 Length of time between first and last PSA value, months .0093 Median (IQR) 12.3(5.2-19.4) 18.6(14.6-22.4) Range 3.0-23.9 3.0-23.9 ⁎ Wilcoxon's test for paired samples. CONCLUSIONS Overall, the PSADT after and before SRT were statistically identical suggesting that after SRT failure, PCa does not emerge with more aggressive biologic features. Further studies are needed to identify predictors and the clinical relevance of individual PSADT changes noted in our study. © 2012 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 187Issue 4SApril 2012Page: e594 Advertisement Copyright & Permissions© 2012 by American Urological Association Education and Research, Inc.MetricsAuthor Information Roberto Muller Durham, NC More articles by this author Joseph Presti Stanford and Palo Alto, CA More articles by this author William Aronson Los Angeles and West Los Angeles, CA More articles by this author Martha Terris Augusta, GA More articles by this author Christopher Kane San Diego, CA More articles by this author Christopher Amling Portland, OR More articles by this author Stephen Freedland Durham, NC More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...