18F-FDG uptake in well-differentiated neuroendocrine tumors correlates with both Ki-67 and VHL pathway inactivation

Introduction: 18FDG PET-scanner positivity correlates with poor prognosis in neuroendocrine neoplasms (NEN). Glucose transporter 1 (GLUT1) and carbonic anhydrase 9 (CA9) are markers of agressivity in tumors. Together with pVHL, they are involved in tumor cell metabolism via the hypoxia-inducible factor (HIF) signaling pathway. The aim of this study was to compare, in a series of well-differentiated neuroendocrine tumors (NET), the 18-FDG uptake and expression of proliferation marker Ki-67, GLUT-1, CA9 and pVHL. Patients and Methods: this retrospective study included 27 patients with a well-differentiated NET. 18FDG PET-scanner imaging were evaluated by the maximum SUV (Standardized Uptake Values). GLUT1, CA9 and pVHL were analyzed by immunohistochemistry. Results: NETs were from pancreatic (n = 19), midgut (n = 4), duodenal (n = 1), esophageal (n = 1), rectal (n = 1) and pulmonary (n = 1) origins. Eight, 11 and 8 tumors were grade 1, 2 and 3 respectively. The mean/median Ki67 was 15/10% [1-60%]. The mean/median SUVmax was 6.2/5.2 [1.4-18.7]. SUVmax correlated with a greater tumor size (p = 0.03), higher expression of Ki-67 (p = 0.04) and low expression of pVHL (p = 0.008). In the group of 16 NET with low proliferative index (Ki-67


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