Relationship between 18F-FDG uptake on PET and various biologic molecular markers in benign pulmonary lesion: comparison with primary lung cancer
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Kyoichi Kaira Yasuhisa Ohde Takehiro Okumura Kazuo Nakagawa Toshiaki Takahashi Haruyasu Murakami Tateaki Naito Asuka Tsuya Yukiko Naka
- چاپ و سال / کشور: 2011
Description
Background Positron emission tomography (PET) imaging with 2-[18F]-fluoro-2-deoxy-D-glucose (18F-FDG) has a false-positive result in benign pulmonary lesions such as granulomatous diseases. The aim of this study was to investigate the underlying biologic mechanisms of 18F-FDG uptake in benign pulmonary lesion. Methods Thirty-five patients with solitary benign pulmonary lesions who underwent 18F-FDG PET were included in this study. Tumor sections were stained by immunohistochemistry for glucose transporter 1 (Glut1); glucose transporter 3 (Glut3); hexokinase I; hypoxiainducible factor-1 alpha (HIF-1a); vascular endothelial growth factor (VEGF); microvessels (CD34); Ki-67; p-Akt; phosph-mammalian target of rapamycin (p-mTOR). 18F-FDG uptake and these biomarkers were evaluated for patients with benign lesion and non-small cell lung cancer (NSCLC). Results A statistically significant correlation in benign pulmonary lesion was observed between 18F-FDG uptake and the expression of Glut1, Glut3, hexokinase I and p-Akt. The degree of 18F-FDG uptake and the expression of Glut1, hexokinase I, HIF-1a, VEGF, CD34, Ki-67 and mTOR were significantly lower in benign pulmonary lesion than NSCLC, but Glut3 expression was significantly higher in benign pulmonary lesion. Glut1, Glut3 and hexokinase I were highly expressed in granulomatous diseases as compared with non-granulomatous diseases. A high uptake of 18F-FDG in benign pulmonary lesion was recognized in patients with the overexpression of Glut1, Glut3, HIF-1a, hexokinase I, VEGF, Ki-67, and Akt. Conclusion The amount of 18F-FDG uptake in benign pulmonary lesion is associated with the presence of glucose transporter (Glut1 and Glut3), glucose phosphorylation (hexokinase I), angiogenesis (VEGF), cell proliferation (Ki-67), and phosphorylation of Akt.
Ann Nucl Med DOI 10.1007/s12149-011-0501-3 Received: 9 March 2011 / Accepted: 19 May 2011
