S1169
Clinical - Urology
ESTRO 2026
trial. Lancet Oncol 2022;23(10):1308-20. doi:10.1016/S1470-2045(22)00517-4 Keywords: SBRT, adverse, events
cystitis) (24%) and urinary retention (20%), followed by haematuria (18%) and urethral stricture (12%).
Digital Poster Highlight 1117 Biomechanistic modeling of PSA dynamics describes personalized prostate cancer response to radiotherapy and androgen deprivation therapy Joaquin Dominguez-Espiñeira 1 , Jane Shortall 2,3 , Vodathi Bamunuarachchi 3 , Alan McWilliam 2,3 , Guillermo Lorenzo 1,4 1 Group of Numerical Methods in Engineering, Department of Mathematics, University of A Coruna, A Coruna, Spain. 2 Division of Cancer Sciences, University of Manchester, Manchester, United Kingdom. 3 The Christie NHS Foundation Trust, The Christie NHS Foundation Trust, Manchester, United Kingdom. 4 Oden Institute for Computational Engineering and Sciences, The University of Texas at Austin, Austin, TX, USA Purpose/Objective: This study aims to design a biomechanistic model that represents the fundamental biological mechanisms underlying the dynamics of prostate cancer (PCa) response and serum prostate-specific antigen (PSA) after external beam radiotherapy (EBRT) and androgen deprivation therapy (ADT) to contribute to early identifying biochemical relapse. Material/Methods: The study was carried out with a retrospective cohort of n=281 patients from a single institution, who received hypofractionated EBRT (50 Gy, 16 doses) either without or with ADT lasting a median (range) of 9 (3, 27) months. Our model consisted of temporally- resolved ordinary differential equations that are solved analytically to obtain a closed form of PSA dynamics before, during, and after treatment [1,2]. We assumed that untreated tumor growth follows exponential growth, that EBRT induces irreversible damage in a fraction of PCa cells (which will ultimately die), and that the complementary fraction survives radiation and continues proliferating. To model ADT, we introduced a split between sensitive PCa cells undergoing treatment-induced death, and resistant cells that continue proliferating. Hence, the model is governed by up to five mechanistic parameters: the tumor cell proliferation rate, the EBRT survival fraction, the EBRT-induced tumor cell death rate, the fraction of ADT resistant cells, and the ADT-induced tumor cell death rate. Together with baseline PSA, these parameters were calibrated via nonlinear least- squares using patient-specific longitudinal PSA series from PCa diagnosis up to maximum patient follow-up
Conclusion: This is the largest single observational study
evaluating SBRT for localised prostate cancer. SBRT was associated with increased GU adverse events but no excess GI adverse events compared with conventional or moderately hypofractionated radiotherapy. The increased risk of GU events did not appear markedly worse than that seen in randomised trials. These findings highlight the need for careful patient selection - particularly among men with pre- existing lower urinary tract symptoms - and provide population-level evidence to inform treatment decisions as SBRT becomes more widely adopted in clinical practice. References: 1.Widmark A, et al. Extreme hypofractionation vs conventionally fractionated radiotherapy for intermediate-risk prostate cancer: early toxicity results from the Scandinavian Phase III HYPO-RT-PC trial. Int J Radiat Oncol Biol Phys 2016;96(5):938-39. doi:10.1016/j.ijrobp.2016.09.0492.As Nv, et al. Phase 3 trial of stereotactic body radiotherapy in localized prostate cancer. N Engl J Med 2024;391(15):1413-25. doi:10.1056/NEJMoa24033653.Tree AC, et al. IMRT vs SBRT for prostate cancer (PACE-B): 2-year toxicity results from a randomized Phase 3 non-inferiority
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