Real-World Treatment Outcomes in Patients With Ga68-PSMA-PET Positive Metastatic Hormone-Sensitive Prostate Cancer With or Without Conventional Imaging Correlates
Background Prostate-specific membrane antigen (PSMA) positron emission tomography (PET) imaging is highly sensitive, enabling detection of disease not visualized on conventional imaging, and leading to a new disease state: PSMA-avid/CT-negative metastatic prostate cancer. The optimal management and treatment outcomes for this group remain poorly defined. We investigated whether treatment intensification with androgen receptor signaling inhibitors (ARSI) provides additional benefit for these patients. Methods We conducted a retrospective study of patients with metastatic hormone-sensitive prostate cancer (mHSPC) diagnosed via standard-of-care PSMA PET/CT imaging (Ga68 gozetotide/PSMA-11) at our institution. Patients were stratified based on whether PSMA-avid lesions (SUVmax > 2.5) had correlates on conventional imaging: PSMA (+)/CT (−) versus PSMA (+)/CT (+). We compared prostate-specific antigen progression-free survival (PSA PFS) and castration resistance-free survival (CRFS) between cohorts. OS was not assessed. Results Among 159 patients, 81 (51%) had PSMA (+)/CT (−) and 78 (49%) had PSMA (+)/CT (+) disease. With a median follow up of 23 months, patients with PSMA (+)/CT (−) mHSPC had significantly longer PSA PFS (hazard ratio [HR] 0.31, P = .01) and CRFS (HR 0.08, P < .001). Within the PSMA (+)/CT (−) cohort, ARSI intensification did not improve CRFS compared to androgen deprivation therapy (ADT) monotherapy (HR 0.32, P = .33). Conclusions Patients with PSMA (+)/CT (−) mHSPC exhibit a more favorable prognosis with reduced risk of PSA progression and castration resistance compared to those with PSMA (+)/CT (+) disease. However, among patients treated with ADT alone, CRFS was similar across groups, suggesting that the benefit of ARSI intensification in PSMA (+)/CT (−) patients requires prospective validation.
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- Oncology & Carcinogenesis
- 3211 Oncology and carcinogenesis
- 1117 Public Health and Health Services
- 1112 Oncology and Carcinogenesis
Citation
Published In
DOI
EISSN
ISSN
Publication Date
Volume
Issue
Related Subject Headings
- Oncology & Carcinogenesis
- 3211 Oncology and carcinogenesis
- 1117 Public Health and Health Services
- 1112 Oncology and Carcinogenesis