2214 Postoperative Nomogram Predicting the 9-Year Probability of Prostate Cancer Recurrence AfterPermanent Prostate Brachytherapy

L. Potters1, R. G. Stock2, J. P. Ciezki3, B. J. Davis4, M. J. Zelefsky5, M. Roach6, N. N. Stone2, P. A. Fearn5, M. W.Kattan7

1New York Prostate Institute at South Nassau Communities Hospital, Oceanside, NY, 2Mount Sinai School of Medicine,New York, NY, 3Cleveland Clinic, Cleveland, OH, 4Mayo Clinic, Rochester, MN, 5Memorial Sloan Kettering CancerCenter, New York, NY, 6University of California at San Francisco, San Francisco, CA, 7Cleveland Clinic Foundation,Cleveland, OH

Purpose/Objective(s): A preoperative nomogram for prostate cancer recurrence after permanent prostate brachytherapy (PPB)has been independently validated as accurate and discriminating. We have developed two PPB post-implant nomograms withoutcomes extending the predictions to 9 years; one using the D90 dose (the minimum dose 90% of the prostate) and the secondusing biological equivalent dose (BED) calculations which provide a method of comparing different isotopes and combinedtherapies.

Materials/Methods: Cox regression analysis was used to model the clinical information for 5,889 patients who underwent PPBfor clinically-localized prostate cancer from six centers. The model was validated against the dataset using bootstrapping.Disease progression was defined as any post-treatment administration of androgen deprivation, a clinical relapse, or abiochemical failure defined as 3 PSA rises. Patients with fewer than 3 PSA rises were censored at the time of the first PSA rise.The BED was calculated from the D90 and EBRT dose using an alpha/beta of 2.

Results: The 9-year progression-free probability for the modeling set was 82% (95% CI, 79% to 84%). In one Cox model, PSA,biopsy Gleason sum, BED, and clinical stage were associated with recurrence (each P �0.05) while, treatment year was not.The concordance index of the nomogram was 0.72. In a second Cox model, PSA, clinical stage, Gleason sum, Isotope, externalbeam radiation, D90 dose were associated with recurrence (each P �0.05) while clinical stage was not. The concordance indexof the nomogram was 0.72.

Conclusions: We have developed and validated as a robust predictive model two post-implant nomograms for prostate cancerrecurrence after PPB. Both nomograms confer the significance of implant dosimetry for predicting outcome. Unique topredictive models, the nomogram predictions can be adjusted for the disease-free interval that a patient has achieved after PPB..

Author Disclosure: L. Potters, None; R.G. Stock, Bard, F. Consultant/Advisory Board; J.P. Ciezki, None; B.J. Davis, Oncura,Inc, F. Consultant/Advisory Board; Calypso Inc, F. Consultant/Advisory Board; Tomotherapy Inc, G. Other; M.J. Zelefsky,None; M. Roach, None; N.N. Stone, Prologics, LLC, E. Ownership Interest; P.A. Fearn, None; M.W. Kattan, OncovanceTechnologies, E. Ownership Interest; Oncovance Technologies, F. Consultant/Advisory Board.

2215 Does Testosterone Influence Radiation-Induced Toxicity In Radiotherapy of the Prostate? A SecondaryAnalysis of RTOG Protocol 9413

D. Taussky1, K. Bae2, J. Bahary1, M. Roach3, C. A. Lawton4, W. U. Shipley5, H. M. Sandler6

1Department of Radiation Oncology, Montreal University, Montreal, PQ, Canada, 2Department of Biostatistics, RTOG,Philadelphia, PA, 3Department of Radiation Oncology, University of California, San Francisco, CA, 4Department ofRadiation Oncology, Medical College of Wisconsin, Milwaukee, WI, 5Department of Radiation Oncology, MassachusettsGeneral Hospital, Boston, MA, 6Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor,MI, Canada

Background: Androgen deprivation in combination with radiotherapy may increase rectal toxicity, as has been suggested inseveral retrospective studies, all with different timing of androgen deprivation.

Purpose/Objective(s): We conducted a secondary analysis of RTOG 9413 to examine if testosterone levels may influenceradiation induced toxicity.

Materials/Methods: We analyzed 2 out of 4 arms of RTOG 9413. These included the 2 arms that treated the whole pelvisfollowed by a boost to the prostate with radiation therapy (RT) and excluded the two arms that received RT to the prostate only.Patients in the two arms differed solely in the timing of 4 months of total androgen deprivation (TAD): arm I (320 patients),TAD was begun 2 months before the start of radiotherapy and continued during radiotherapy (concomitant). In arm III (319patients), TAD started immediately after the completion of radiotherapy (adjuvant). Time to testosterone recovery wascalculated from either the end of radiotherapy (concomitant arm) or starting 4 months after the completion of radiotherapy(adjuvant arm). Acute and late rectal and acute urinary toxicity (CTC v.2.0) were modeled using the multivariate logisticregression and the multivariate Cox-proportional hazards regression.

Results: Median follow up for all patients is 6.0 and 5.8 years (arm I and III, resp.). Median age was 70y in both arms. Thefrequency of late rectal toxicity (grade 0–1 vs. 2–5, p�0.2166) and late urinary toxicity (grade 0–1 vs. 2–5, p�0.4203) are notstatistically significantly different between the two arms. 80.0 % and 79.9% (arm I and III, resp.) of patients had normal baselinetestosterone levels and 33.1% and 30.1% did not have a return to normal testosterone levels. Time to testosterone recovery for

S329Proceedings of the 48th Annual ASTRO Meeting