3247 - Effect of Prostate-Specific Membrane Antigen PET/CT Guidance on Metastasis-directed Radiotherapy for Oligometastatic Castration-Resistant Prostate Cancer
Presenter(s)
J. Chojnowski1, A. Pepin1, C. Friedes1, D. Shin2, A. Castellanos3, A. Farolfi4, J. P. Christodouleas1,5, A. Goel1, N. Nichols6, M. L. Steinberg7, A. U. Kishan8, J. Czernin9, J. Calais9, N. Vapiwala1, and J. Nikitas1; 1Department of Radiation Oncology, University of Pennsylvania, Philadelphia, PA, 2Drexel University College of Medicine, Philadelphia, PA, 3UCLA, Los Angeles, CA, 4Ahmanson Translational Theranostics Division, UCLA Nuclear Medicine, Los Angeles, CA, 5Elekta, Stockholm, Sweden, 6VA and UCLA, Los Angeles, CA, 7Department of Radiation Oncology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 8Department of Radiation Oncology, University of California, Los Angeles, Los Angeles, CA, 9Department of Nuclear Medicine and Theranostics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA
Purpose/Objective(s): Patients with metastatic castration-resistant prostate cancer (mCRPC) have limited systemic therapy options, often with associated toxicity. Starting a new line of systemic therapy may not be warranted in cases of oligoprogressive disease amenable to metastasis-directed radiotherapy (RT). In parallel, prostate-specific membrane antigen (PSMA) PET/CT allows for higher sensitivity in detecting metastatic disease than conventional imaging. We hypothesized that metastasis-directed RT can offer durable disease control in mCRPC patients with a limited number of metastatic sites and that the use of PSMA PET/CT would be associated with improved outcomes.
Materials/Methods: Patients were screened from prospective and retrospective databases at two large academic centers. Inclusion criteria included having a diagnosis of mCRPC, having up to 5 sites of new or progressive disease, and receiving metastasis-directed RT to all sites. Castration resistance was defined as 2 consecutive prostate-specific antigen [PSA] increases or radiographic progression with testosterone <50 ng/dL. Progression-free survival (PFS) and overall survival (OS) were calculated from the start of metastasis-directed RT using the Kaplan-Meier method. Progression was defined as biochemical progression (PSA increase >2 ng/mL above nadir) or radiographic progression. Cox regression was used to compare PFS, adjusting for age, stage (N1/M1a vs M1b vs M1c), and number of treated sites (1 vs 2/3).
Results: Fifty-one patients met inclusion criteria. Median follow-up was 35.4 mo (IQR 25.5-45.3). Median age was 69 years (IQR 65-74). Median PSA was 2.0 ng/mL (IQR 0.8-4.3). Initial treatment consisted of prostatectomy (32, 62.7%), prostate RT (14, 27.5%), or systemic therapy (5, 9.8%). Median time between castration resistance and RT was 13.7 mo (IQR, 4.6-26.3). Patients were restaged using PSMA PET/CT (31, 60.8%), fluciclovine PET/CT (8, 15.7%), bone scan (4, 7.8%), or CT/MRI (3, 5.9%). Patients had N1M0 (10, 19.6%), M1a (9, 17.6%), M1b (30, 58.8%), or M1c (2, 3.9%) disease. Patients were treated to 1 (27, 52.9%), 2 (16, 31.4%), or 3 (8, 15.7%) sites. Concurrent treatment included androgen deprivation therapy (ADT) (13, 25.5%), ADT plus androgen receptor pathway inhibitor (ARPI) (31, 60.8%), ARPI (3, 5.9%), ADT plus chemotherapy (1, 2%), or none (1, 2%). Median PFS was 15.3 mo (95% CI, 10.8-22.2). 3-year OS was 85.2% (95% CI, 77.1-100%). PSMA PET/CT was associated with improved PFS (HR 0.51 [95% CI: 0.25-1.01], p=0.056). Multiple treated sites (HR 1.94) and stage (HR 1.93 for M1b; HR 28.3 for M1c) were associated with worse PFS.
Conclusion: For patients with oligometastatic CRPC, metastasis-directed RT can offer durable disease control, deferring new lines of systemic therapy. PSMA PET/CT guidance appears to improve PFS outcomes, likely due to better identification of metastases.