Abstract Book

S259

ESTRO 37

high-risk patients (CF 199, HF 192) with >4yr follow-up. Biochemical or clinical failure within 5 years was scored (CF 58, HF 50). A 3D mapping of dose surrounding the prostate was defined such that locations correspond which lie in a given direction relative to the center of mass of the delineated prostate, at a given relative distance to or absolute distance outside its surface. Mean dose maps were computed for patients without and with failure, and dose difference maps constructed. Per-pixel student’s t-tests were performed, and contours drawn around regions with p<0.05 and p<0.01. Based on the observed differences, dose in a point at 2.5cm distance to the prostate towards the obturatorial region was collected, and Kaplan Meier curves constructed. Results Figure 1a shows dose differences by FFF for the CF patients, mapped to the anatomy of an arbitrary patient. Regions with positive dose differences and low p-values were observed surrounding the prostate. Near to and inside the prostate, regions with low p had small negative dose differences (up to -1Gy), possibly associated with more heterogeneous (higher) PTV dose for highly conformal distributions with lower dose outside the prostate. For patient subgroups based on dose cutoff values of 50Gy and 60Gy in the obturatorial point, figure 1b shows significantly different FFF curves. For the HF patients dose differences were smaller, with only few pixels reaching p<0.01 (not shown). These diverging observations between the randomization arms confirm that the underlying mechanism for the CF dose differences depends on the delivered dose and its fractionation. Assuming that identified dose difference regions correlate with subclinical involvement, investigations into biological fractionation effects for subclinical disease would be warranted. Estimations of tumor α/β based on biochemical or clinical failure in trials including high-risk patients could be biased due to the influence of such subclinical disease.

population treated with CF IG-IMRT. For HF treatment the association did not hold. OC-0502 Testosterone recovery following androgen deprivation and radiation therapy for prostate cancer D. Spiegel 1 , J. Hong 1 , T. Oyekunle 2 , W. Lee 1 , J. Salama 1 , B. Koontz 1 1 Duke University Medical Center, Radiation Oncology, Durham- NC, USA 2 Duke University Medical Center, Statistics, Durham- NC, USA Purpose or Objective Concurrent androgen deprivation therapy (ADT) and radiation therapy (RT) is a frequently used prostate cancer (PC) treatment. Testosterone recovery (TR) after ADT-RT is not well-characterized. We studied TR in men who received RT and either short-term (ST) or long-term (LT) ADT with LHRH agonists. Material and Methods We identified consecutive localized PC patients treated with ADT-RT at the Durham VA Medical Center (DVAMC) and Duke University Medical Center (DUMC) from 1/2011- 10/2016 with a documented baseline testosterone (T) level. TR was defined as time from last ADT injection to T normalization (lower lab limit: 240 ng/dL for DVAMC and 175 ng/dl for DUMC). The Kaplan-Meier method was used to estimate median time to TR and biochemical progression-free survival (BFPS). Cox proportional hazards models were generated to identify TR predictors with a nomogram built from DVAMC data based on a parsimonious multivariate model. As an internal validation measure, the bias-corrected concordance index (c-index) for the nomogram was obtained from 1000 bootstrap resamples. The nomogram was then externally validated with DUMC patients. Results 340 patients were included from DVAMC and DUMC. 70% were treated with STADT, median duration 6 months; 30% were treated with LTADT, median duration 24.3 months. Median follow-up was 26.7 months. Median age was 65 (range 42-91). Prior to treatment, 73.5% had normal baseline T. Median time for TR was 18.3 months for all patients (17.2 for STADT and 24.0 months for LTADT, p = 0.004). The cumulative incidence of testosterone recovery at 2 years was 53.1% (95% CI 38.2-69.6) after LTADT compared to 65.7% (95% CI 58.7-72.7) after STADT (p=0.004). LTADT patients had longer castrate T duration than STADT patients (9.7 months vs 6.9 months, p=0.001). There was no statistically significant difference in 2-year BPFS between ST and LT ADT cohorts (97.3% vs 96.7%, p=0.524). On multivariate analysis, higher pre- treatment T (HR = 1.005 95% CI 1.003-1.006, p<0.001), use of STADT (HR = 2.63 95% CI 1.49-4.55, p<0.001), and lower BMI (HR = 0.94 95% CI 0.91-0.97, p<0.001) were associated with shorter time to TR. Older age (HR = 0.97 95% CI 0.93-1.00, p = 0.05) and white race (HR = 0.67 95% CI 0.44-1.03, p = 0.07) trended as longer TR predictors. Smoking status and Charlson Comorbidity Index were not significant independent TR predictors. A nomogram was generated to predict probability of TR at 1, 2, and 3 years. The c-index was 0.73 (95% CI 0.71-0.75) for the original DVAMC data set and 0.72 (95% CI 0.65-0.77) for the DUMC validation set.

Conclusion We confirmed an association between dose delivery outside the prostate and FFF in a recent patient