PET Imaging of Glutaminolysis in Tumors by 18F-(2S,4R)4-Fluoroglutamine

Gliosarcoma Glutaminolysis
DOI: 10.2967/jnumed.111.093815 Publication Date: 2011-11-16T16:58:13Z
ABSTRACT
Changes in gene expression, metabolism, and energy requirements are hallmarks of cancer growth self-sufficiency. Upregulation the PI3K/Akt/mTor pathway tumor cells has been shown to stimulate aerobic glycolysis, which enabled <sup>18</sup>F-FDG PET imaging. However, millions scans conducted per year, a significant number malignant tumors PET–negative. Recent studies suggest that several may use glutamine as key nutrient for survival. As an alternative metabolic tracer tumors, <sup>18</sup>F-(<i>2S,4R</i>)4-fluoroglutamine was developed mapping glutaminolytic tumors. <b>Methods:</b> A series vitro cell uptake vivo animal were performed demonstrate addiction glutamine. Cell this SF188 9L glioblastoma cells. Dynamic small-animal 2 models: xenografts produced F344 rats by subcutaneous injection transgenic mice with M/tomND spontaneous mammary gland <b>Results:</b> In showed both transformed displayed high rate (maximum uptake, ≈16% dose/100 μg protein). The is comparable <sup>3</sup>H-l-glutamine but higher than <sup>18</sup>F-FDG. can be selectively blocked. Biodistribution localized surrounding muscle liver tissues. Data certain production. <b>Conclusion:</b> results support taken up trapped It useful novel
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