644 Background: Serum pancreastatin, a cleave product of chromogranin A, has shown promise as a prognostic and predictive biomarker in neuroendocrine tumors (NETs) undergoing surgical cytoreduction or liver-directed therapies. However, its role as a predictive biomarker among patients undergoing Peptide Receptor Radionuclide Therapy (PRRT) has not been investigated. We sought to retrospectively analyze the role of pancreastatin as a biomarker for outcomes among patients with advanced NETs who received treatment with PRRT at our institution. Methods: An IRB-approved prospective institutional NET registry (2018-2024) was used to identify and include patients who received at least 3 cycles of Lu177-DOTATATE and had serum pancreastatin levels measured within 100 days before and after PRRT. Patient demographics, tumor grade and site of origin, pancreastatin levels and therapies received before and after PRRT and outcomes were abstracted. Cox regression was used to evaluate the ability of the post-treatment change in pancreastatin to predict progression-free survival (PFS). Predictive performance was estimated using Uno’s C-statistic and statistically compared to a null value of 0.50. Standard errors were computed using 100 perturbation samples. All statistical testing was two-sided and assessed for significance at the 5% level using SAS v9.4 (SAS Institute, Cary, NC). Results: 162 patients received PRRT, of which 49 patients met criteria for inclusion. The majority of patients had small bowel (n=29, 61.7%) and pancreatic NETs (n=14, 29.8%). Median PFS for the entire cohort was 30.2 months. The mean and median change in serum pancreastatin before and after PRRT was 196.8 pg/ml and -103 pg/ml, respectively. On univariate analysis, the post-treatment change in serum pancreastatin was not found to have a C-index significantly greater than 0.50 (Concordance=0.52, p=0.66). Results were consistent when dichotomizing according to the first quartile (p=0.38), median (p=0.91), and third quartile (p=0.97), indicating that the post-treatment change in serum pancreastatin was not found to be predictive of the risk of progression or death. The predictive effect of serum pancreastatin did not significantly differ according to site of origin in an interaction analysis (p=0.77). Conclusions: In this single-institution analysis, changes in serum pancreastatin before and after treatment were not predictive of progression-free survival across analytic thresholds or sites of origin. Although prospective data are needed to validate these findings, our findings do not support the routine use of pancreastatin among patients undergoing treatment with PRRT.
Gao et al. (Sat,) studied this question.