C.R. Williams

PROTON RADIOTHERAPY FOR PROSTATE CANCER IS NOT ASSOCIATED WITH POST-TREATMENT TESTOSTERONE SUPPRESSION

PURPOSE Three independent studies of photon (x-ray) radiotherapy (RT) for prostate cancer have demonstrated evidence of testosterone suppression after treatment. The present study was undertaken to determine whether this would also be the case with conformal protons. METHODS AND MATERIALS Between August 2006 and October 2007, 171 patients with low- and intermediate-risk prostate cancer were enrolled and underwent treatment according to the University of Florida Proton Therapy Institute institutional review board-approved PR01 and PR02 protocols. Of the 171 patients, 18 were excluded because they had received androgen deprivation therapy either before (n = 17) or after (n = 1) RT. The pretreatment serum testosterone level was available for 150 of the remaining 153 patients. These 150 patients were included in the present study. The post-treatment levels were compared with the pretreatment levels. RESULTS The median baseline pretreatment serum testosterone level was 357.9 ng/dL. The median post-treatment testosterone value was 375.5 ng/dL at treatment completion (p = .1935) and 369.9 ng/dL (p = .1336), 348.7 ng/dL (p = .7317), 353.4 ng/dL (p = .6996), and 340.9 ng/dL (p = .1669) at 6, 12, 18, and 24 months after proton therapy, respectively. CONCLUSIONS Conformal proton therapy to the prostate, as delivered using the University of Florida Proton Therapy Institute PR01 and PR02 protocols, did not appear to significantly affect the serum testosterone levels within 24 months after RT.

Image-Guided Proton Therapy for Low- and Intermediate-Risk Prostate Cancer: Three-Year Results of Two Prospective Trials

152 Background: To report outcomes in two prospective proton therapy (PT) trials for localized prostate cancer. METHODS From 2006 to 2007, 171 low- and intermediate-risk prostate cancer patients were treated with PT on prospective trials. Low-risk patients (N=89) were treated on PR01 with 78 CGE/39 fractions to the prostate. Intermediate-risk patients (N=82) were treated on PR02, a dose-escalation trial, with 78-82 CGE to the prostate and proximal seminal vesicles. Based on organ-constraint goals, 57 (69%), 13 (16%), and 12 (15%) PR02 patients received 82 CGE, 80 CGE, and 78 CGE, respectively. Toxicity was scored by CTCAE v3 and biochemical failure defined as nadir + 2 ng/mL. RESULTS The proportions of PR01 and 02 patients alive with no evidence of disease are 83 (93%) and 73 (89%); alive with disease, 1 (1%) and 1 (1%); and dead of intercurrent disease, 5 (6%) and 8 (10%), respectively. Only 2 patients had disease progression, both isolated pelvic-node recurrences. No patient died of prostate cancer or recurred locally. Grade (GR) 3 genitourinary (GU) and gastrointestinal (GI) complications occurred in 2 of 101 (2%), 0 of 13, and 4 of 57 (7%) patients receiving 78, 80, and 82 CGE, respectively. GR 3 GU toxicity occurred in 1 PR01 and 3 PR02 patients, including hematuria in 1 PR01 patient on anticoagulation; posttreatment TURP in 2 who had pretreatment (pre-tx) TURP; and dysuria in 1 with severe chronic pre-tx prostatitis. Multivariate analysis (MVA) of protocol, dose, age, prostate volume, pre-tx IPSS, pre-tx medical or surgical GU symptom management (SM), anticoagulation, and bladder wall V70 or V30 showed only pre-tx SM (P< .0001) and age (P =.007) to be associated with GR2+ toxicity. GR 3 GI toxicity occurred in 2 PR02 patients, including rectal bleeding in a patient on anticoagulation, and rectal bleeding and proctitis in a patient on anticoagulation who had a transrectal prostate biopsy. MVA of protocol, age, dose, anticoagulation, and rectal wall V70 or rectum V30 showed only rectal wall V70 (.045) and rectum V30 (.027) to be associated with GR 2+ rectal bleeding and proctitis. CONCLUSIONS PT may provide sufficiently reduced toxicity to permit further dose intensification and/or concomitant chemotherapy.