Abstract
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Introduction: The aim of this retrospective, single-center study was to evaluate whether changes in quantitative PSMA PET metrics following initiation of androgen deprivation therapy (ADT) and / or androgen receptor signaling inhibitor (ARSi) are associated with PSA progression.
Methods: Patients who underwent at least 2 PSMA PET/CT scans (PSMA PET) at UCLA between October 2016 and April 2021 were retrospectively screened for this study. Patients who started a new line of ADT and / or ARSi between PET1 and PET2 were included. The same patient could be included twice in this analysis based on these inclusion criteria. Patients starting any other treatment between the 2 PSMA PET scans and patients lacking follow-up clinical data were excluded. Clinical information was collected from electronic medical records. The study flowchart is shown in Figure 1. Whole-Body Tumor SUVmean and Tumor Volume (PSMA-TV) on PSMA PET were extracted using qPSMA software. miTNM staging was evaluated using PROMISE criteria. The presence of new lesions on PET2 was evaluated by a board-certified nuclear medicine physician. We investigated the association between progression of disease (PD) by PSA (≥25% increase from PSA nadir following initiation of ADT / ARSi) and the following outcomes: PD defined using changes in PSMA-TV (PSMA-TV PD: ≥20% increase), SUVmean (SUVmean PD: ≥30% increase), and the appearance of new lesions on PET2 relative to PET1. PSA Progression-Free Survival (PSA-PFS) was calculated from the time of ADT / ARSi initiation to PSA progression. Kaplan-Meier analysis and log-rank test were used to assess the associations between the exposure time under ADT / ARSi (>12 months vs. <12 months) and the type of treatment initiated after PET1 (ADT vs. ARSi +/- ADT) with PSA-PFS. Spearman’s rank correlation coefficients were generated to evaluate the association of percent changes in PSMA-TV and SUVmean with percent changes in PSA between PET1 and PET2.
Results: A total of 35 patients were included in the analysis. One patient was included twice because he underwent three PET scans and started a new line of ADT / ARSi after PET1 and after PET2. Patient demographics are outlined in Table 1. Table 2 summarizes changes in PSA, miTNM staging, SUVmean, and PSMA-TV between PET1 and PET2. The percent changes between PET1 and PET2 in median serum PSA levels, SUVmean, and PSMA-TV were -85.8%, -22.2%, and -86.9%, respectively. Table 3 summarizes the classification of patients as non-PD or as having no new lesions on PET2 based on PSA progression status at time of PET2. Overall, 19 patients (52.8%) experienced PSA progression at time of PET2, and 17 patients (47.2%) did not. In the latter group, a higher percentage of patients were classified as non-PD based on PSMA-TV (94.1% (16/17) vs. 78.9% (15/19)), SUVmean (94.1% (16/17) vs. 84.2% (16/19)), and new lesion criteria (88.2% (15/17) vs. 63.2% (12/19)) compared to those who progressed at time of PET2. Percent changes in PSA were significantly correlated to percent changes in PSMA-TV and SUVmean between PET1 and PET2, respectively (Spearman ρ: 0.757 and 0.636; p < .001). Kaplan-Meier analysis did not show a statistically significant difference in PSA-PFS between patients who were on ADT < 12 months and patients who were on ADT > 12 months (p = 0.404) and between patients treated with ADT only and those treated with ARSi +/- ADT (p = 0.077) (Figure 2).
Conclusions: Changes in quantitative PSMA PET metrics following initiation of ADT and / or ARSi are strongly correlated with changes in PSA and may be predictive of PSA progression. Limitations of this study include the small cohort size and the retrospective nature of this analysis. Further research is necessary to evaluate the prognostic value of changes in quantitative PSMA PET metrics in patients who undergo treatment with ADT and / or ARSi.
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