Conclusions
SPN cells harbor an active molecular capacity for increased glucose metabolism. Especially, defective type SPNs were associated with low metabolic activity and related to low Ki-67 index.
Methods
mRNA expressions for glucose metabolism were analyzed in five SPNs, five pancreatic ductal adenocarcinomas (PCAs), and paired normal pancreatic tissues. Among the proteins involved in glucose metabolism, the expressions of five proteins (GLUT1, HK1, PFKM, ENO2, and PKM2) were evaluated in 36 SPNs by immunohistochemistry. Clinical patterns of SPN on PET scans were classified according to the proportion of 18F-FDG uptake within the whole tumor volume (hot: ≥ 70%, mixed: 30 ≤ < 70, and defective: < 30%). PET-based parameters, including maximum standardized uptake value (SUVmax) and metabolic tumor volume (TMV2.5), were evaluated.
Objective
We aimed to investigate the metabolic characteristics of Solid pseudopapillary neoplasms (SPNs) in relation signal intensities on 18F-FDG PET scans. Summary background data: SPNs of the pancreas commonly show high uptake of 18F-FDG. However, the metabolic characteristics underlying the high 18F-FDG uptake in SPNs are not well characterized. Materials and
Results
Hot (n = 19), mixed (n = 5), and defective (n = 12) 18F-FDG uptake patterns were noted in the 36 patients. Radiologic tumor size and SUVmax differed significantly according to these patterns (ANOVA, p < 0.05). GLUT1, HK1, PFKM, ENO2, and PKM2 were highly expressed in SPNs at both the mRNA and protein levels. Defective type SPNs showed lower expression of HK1 (p = 0.014), PKM2 (p = 0.028), and Ki-67 (p = 0.070) with frequent intra-tumoral necrosis (p = 0.007). High Ki-67 expression (≥ 3%) was associated with high SUVmax in pancreatic SPNs (p = 0.002). Conclusions: SPN cells harbor an active molecular capacity for increased glucose metabolism. Especially, defective type SPNs were associated with low metabolic activity and related to low Ki-67 index.