S1208
Clinical - Urology
ESTRO 2026
Median TTN was also shorter with boosting, at 2.15 months versus 3.75 months (p=0.033). For patients with PI-RADS ≤ 4 lesions, IPL boosting did not significantly influence PSA kinetics. Mean PSA nadir was 0.070ng/mL in the boost group (n=43) and 0.050ng/mL in the no-boost group (n=35) (p=0.115). Median TTN was 4.0 months and 3.2 months, respectively (p=0.9).
Digital Poster Highlight 2002
Intraprostatic Lesion Boost Enhances PSA Kinetics in High PI-RADS Prostate Cancer Treated with MR- Guided SBRT Darren MC Poon 1 , JING YUAN 2 , Oi Lei Wong 2 , Bin Yang 3 , Hiu Yi Wong 2 , Sin Ting Chiu 4 , George Chiu 4 , Ben Yu 3 1 Comprehensive Oncology Centre, Hong Kong Sanatorium and Hospital, Happy Valley, Hong Kong. 2 Research Department, Hong Kong Sanatorium and Hospital, Happy Valley, Hong Kong. 3 Medical Physics Department, Hong Kong Sanatorium and Hospital, Happy Valley, Hong Kong. 4 Department of Radiotherapy, Hong Kong Sanatorium and Hospital, Happy Valley, Hong Kong Purpose/Objective: MR–guided SBRT (MRgSBRT) permits daily soft-tissue visualization and online adaptation, enabling accurate intraprostatic lesion (IPL) targeting. Whether MRI- defined IPL boosting translates into measurable biological response remains insufficiently characterized. Prostate-specific antigen (PSA) nadir and time-to-nadir (TTN) serve as early surrogate markers of tumor ablation and long-term biochemical control. This study for the first time evaluates the impact of IPL boost on PSA kinetics in patients undergoing 5-fraction MRgSBRT, stratified by PI-RADS score, to identify patients who derive meaningful benefit from focal dose escalation. Material/Methods: A prospective cohort of localized prostate cancer patients treated on a 1.5T MR-LINAC was analyzed. Patients received 36.25–40Gy in 5 fractions to the prostate; MRI-visible IPLs (PI-RADS 3–5) were boosted to 40–42.5Gy. IPLs were delineated on diagnostic T2W/DWI sequences. Online Adapt-to-Position or Adapt-to-Shape workflows were used. Androgen- deprivation therapy was prescribed at clinician discretion. PSA was measured at 1-month and subsequently every 3–6 months, predominantly with ultra-sensitive assays (detection limit ~0.003ng/mL). PSA nadir and TTN were analyzed using Wilcoxon and log-rank tests, with stratification by PI-RADS_max (5 vs ≤ 4). Results: 166 patients were included (boost/no-boost n=79/87) with a median follow-up of 24 months (range: 1–63). Baseline characteristics were balanced between groups (all p>0.05). PSA nadir was achieved in 84.8% and 82.7% of patients in the boost and no-boost cohort, respectively. Among patients with PI-RADS5 lesions, IPL boosting was associated with significantly more favorable PSA kinetics. The mean PSA nadir was 0.054ng/mL in the boost group (n=24) compared with 0.173 ng/mL in the no-boost group (n=32) (p=0.034).
Conclusion: IPL boosting during MRgSBRT is associated with significantly more favorable PSA kinetics in PI-RADS5 prostate cancer. These findings suggest that high- grade PI-RADS lesions exhibit a distinct biological response to focal intensification, whereas lower PI- RADS lesions show limited incremental benefit. This phenotype-driven divergence underscores the importance of selective patient stratification in intraprostatic dose escalation. The results support a precision-boost strategy guided by MRI and justify prospective evaluation of long-term biochemical control in future MR-LINAC–based trials. Keywords: Prostate cancer, PSA kinetics, IPL boost
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