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// Minhee Park 1, * , Ho Kyoung Hwang 2, 4, * , Mijin Yun 3, 4 , Woo Jung Lee 2, 4 , Hoguen Kim 1 and Chang Moo Kang 2, 4 1 Departments of Pathology and BK21 PLUS for Medical Science, Yonsei University College of Medicine, Seoul, Korea 2 Department of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Yonsei University College of Medicine, Seoul, Korea 3 Department of Nuclear Medicine, Yonsei University College of Medicine, Seoul, Korea 4 Pancreatobiliary Cancer Clinic, Yonsei Cancer Center, Severance Hospital, Seoul, Korea * These authors contributed equally to this work Correspondence to: Hoguen Kim, email: hkyonsei@yuhs.ac Chang Moo Kang, email: cmkang@yuhs.ac Keywords: solid pseudopapillary neoplasm; metabolomics; metabolism; 18 F-FDG-PET; pancreatectomy Received: October 05, 2017 Accepted: November 14, 2017 Published: January 03, 2018 ABSTRACT Objective: We aimed to investigate the metabolic characteristics of Solid pseudopapillary neoplasms (SPNs) in relation signal intensities on 18 F-FDG PET scans. Summary Background Data: SPNs of the pancreas commonly show high uptake of 18F-FDG. However, the metabolic characteristics underlying the high 18 F-FDG uptake in SPNs are not well characterized. Materials and 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 18 F-FDG uptake within the whole tumor volume (hot: ≥ 70%, mixed: 30 ≤ < 70, and defective: < 30%). PET-based parameters, including maximum standardized uptake value (SUV max ) and metabolic tumor volume (TMV 2.5 ), were evaluated. Results: Hot ( n = 19), mixed ( n = 5), and defective ( n = 12) 18 F-FDG uptake patterns were noted in the 36 patients. Radiologic tumor size and SUV max 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 SUV max 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.
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