3207 - PSA Response to Neoadjuvant Androgen Deprivation Therapy (NA-ADT) and Long-Term Cancer Outcomes in Men Treated with Definitive External Beam Radiotherapy (EBRT) and High Dose Rate Brachytherapy Boost (HDRBT)

12:45pm - 02:00pm PT

Hall F

Screen: 10

POSTER

Presenter(s)

Marcus Cheng, MD, BBiomed - Alfred Health Radiation Oncology, Melbourne, VIC

M. Cheng¹, T. Kang^1,2, J. Bensley³, J. L. Millar^1,2, and W. L. Ong^1,2; ¹Alfred Health Radiation Oncology, Melbourne, VIC, Australia, ²School of Translational Medicine, Monash University, Melbourne, Australia, ³Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Melbourne, VIC, Australia

Purpose/Objective(s):

Suboptimal PSA response to NA-ADT may portend a poorer cancer outcome in men treated with EBRT. The aim of our study was to investigate PSA response to NA-ADT as a prognostic factor in a cohort of men with prostate cancer who had definitive EBRT along with treatment intensification with HDRBT.

Materials/Methods:

This was a single institutional retrospective study of all men with NCCN intermediate risk (IRPC) to high risk (HRPC) prostate cancer who had EBRT+HDRBT, between 1998 and 2024. All men had 6 months NA-ADT, and men with high-risk prostate cancer had a further 2-year adjuvant ADT. Only men who had a repeat PSA prior to EBRT+HDRBT were included in the analyses. Poor PSA response was defined as PSA >0.5 ng/mL prior to EBRT+HDRBT. Cox regression and Fine-Gray models were used to test whether poor PSA response was associated with biochemical recurrence (BCR), metastases free survival (MFS), prostate cancer specific survival (PCSS), and overall survival (OS). Multivariable analyses were performed adjusting for ISUP Grade Group, PSA at diagnosis, clinical T categories, and duration of ADT.

Results:

Of the 550 men who had EBRT+HDRBT in our database, there were 445 men who had PSA prior to EBRT+HDRBT and included this analysis. The median PSA prior to EBRT-HDRBT was 11.3 ng/mL (IQR: 7.3-18.95). There were 199 (44%) and 249 (56%) men who had PSA <0.5 ng/mL and PSA >0.5 ng/mL prior to EBRT+HDRBT respectively. The median follow-up for the cohort was 14.4 years (IQR: 9-18.5 years). The 10-year cumulative incidence of BCR was 20.2% (95%CI=15-27%) for patients with PSA <0.5 ng/mL and 29.7% (95%CI=24-36.3%) for patients with PSA >0.5 ng/mL (P=0.007). The 10-year MFS was 92.7% (95%CI=88.2-95.6%) for patients with PSA <0.5 ng/mL and 96.2% (95%CI=91.7-98.3%) for patients with PSA >0.5 ng/mL (P=0.0012). The 10-year PCSS was 79.6% (95%CI=73.2-84.7%) for patients with PSA <0.5 ng/mL and 80.9% (95%CI=75.2-85.4%) for patients with PSA >0.5 ng/mL (P=0.60). The 10-year OS was 93.2% (95%CI=88.3-96.1%) for patients with PSA <0.5 ng/mL and 84.4% (95%CI=78.8-88.6%) for patients with PSA >0.5 ng/mL (P=0.005). In multivariable analyses, after adjusting for pre-defined covariables, PSA<0.5ng/mL was associated with lower BCR (sHR=0.75; 95%CI=0.39-0.85; P=0.006), but not DMFS (HR=1.23; 95%CI=0.70-2.15; P=0.468), PCSM (HR=0.74; 95%CI=0.41-1.29; P=0.287) and OS (HR=0.91; 95%CI=0.68-1.21; P=0.503).

Conclusion:

In this single-institutional cohort of men with treated with NAADT+EBRT+HDRBT, we confirmed that poor PSA response (>0.5 ng/mL) with NAADT was associated with increased risk of BCR.