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. 2012 Sep;81(9):2423-9.
doi: 10.1016/j.ejrad.2011.09.017. Epub 2011 Nov 4.

18F-FDG uptake on PET in primary mediastinal non-thymic neoplasm: a clinicopathological study

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18F-FDG uptake on PET in primary mediastinal non-thymic neoplasm: a clinicopathological study

Kyoichi Kaira et al. Eur J Radiol. 2012 Sep.

Abstract

Background: The usefulness of 2-[(18)F]-fluoro-2-deoxy-D-glucose ((18)F-FDG) positron emission tomography (PET) has been investigated in thymic epithelial tumors. However, little is known about PET imaging of (18)F-FDG in primary non-thymic mediastinal neoplasms. The aim of this study is to explore the clinicopathological significance of (18)F-FDG PET in primary mediastinal (non-thymic) neoplasms.

Methods: Twenty-one patients with mediastinal neoplasms who underwent (18)F-FDG PET before treatment were included in this study. Tumor sections were stained by immunohistochemistry for glucose transporter 1 (Glut1); glucose transporter 3 (Glut3); hypoxia-inducible factor-1 alpha (HIF-1α); hexokinase I; vascular endothelial growth factor (VEGF); microvessels (CD34); epidermal growth factor receptor (EGFR); Akt/mTOR signaling pathway (p-Akt and p-mTOR); cell cycle control (p53).

Results: Seventeen of 21 patients were imaged on PET system using (18)F-FDG, but 4 patients with a histology of cyst showed nothing abnormal in PET scans. The histology of the resected tumors was as follows: 6 schwannoma, 3 teratoma, 4 cyst, 3 sarcoma, 1 undifferentiated carcinoma, 1 seminoma, 1 mediastinal goiter, 1 ganglioneuroma, and 1 Hodgkin lymphoma. (18)F-FDG uptake was significantly correlated with Glut1, HIF-1α, EGFR, p-Akt and p-S6K. These biomarkers were highly expressed in schwannoma, teratoma and high grade malignancies, whereas all patients with cyst and ganglioneuroma had no positive expression of these biomarkers. High uptake of (18)F-FDG was significant associated with Glut1, VEGF, EGFR, p-Akt, p-S6K and tumor maximal size.

Conclusion: The amount of (18)F-FDG uptake in primary mediastinal non-thymic neoplasms is determined by the presence of glucose metabolism (Glut1), hypoxia (HIF-1α) and upstream components of HIF-1α (EGFR, p-Akt and p-S6K).

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