Metabolic characteristics of solid pseudopapillary neoplasms of the pancreas

Their relationships with high intensity 18F-FDG PET images

Minhee Park, Ho Kyoung Hwang, Mijin Yun, Woo Jung Lee, Hoguen Kim, ChangMoo Kang

Research output: Contribution to journalArticle

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Abstract

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 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. 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.

Original languageEnglish
Pages (from-to)12009-12019
Number of pages11
JournalOncotarget
Volume9
Issue number15
DOIs
Publication statusPublished - 2018 Jan 1

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Fluorodeoxyglucose F18
Pancreatic Neoplasms
Neoplasms
Tumor Burden
Glucose
Positron-Emission Tomography
Glucose Transporter Type 1
Messenger RNA
Analysis of Variance
Proteins
Adenocarcinoma
Necrosis
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Oncology

Cite this

Park, Minhee ; Hwang, Ho Kyoung ; Yun, Mijin ; Lee, Woo Jung ; Kim, Hoguen ; Kang, ChangMoo. / Metabolic characteristics of solid pseudopapillary neoplasms of the pancreas : Their relationships with high intensity 18F-FDG PET images. In: Oncotarget. 2018 ; Vol. 9, No. 15. pp. 12009-12019.
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abstract = "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 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. 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.",
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Metabolic characteristics of solid pseudopapillary neoplasms of the pancreas : Their relationships with high intensity 18F-FDG PET images. / Park, Minhee; Hwang, Ho Kyoung; Yun, Mijin; Lee, Woo Jung; Kim, Hoguen; Kang, ChangMoo.

In: Oncotarget, Vol. 9, No. 15, 01.01.2018, p. 12009-12019.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Metabolic characteristics of solid pseudopapillary neoplasms of the pancreas

T2 - Their relationships with high intensity 18F-FDG PET images

AU - Park, Minhee

AU - Hwang, Ho Kyoung

AU - Yun, Mijin

AU - Lee, Woo Jung

AU - Kim, Hoguen

AU - Kang, ChangMoo

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N2 - 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 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. 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.

AB - 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 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. 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.

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