Published online Nov 28, 2016. doi: 10.4329/wjr.v8.i11.880
Peer-review started: June 9, 2016
First decision: July 30, 2016
Revised: August 24, 2016
Accepted: September 13, 2016
Article in press: September 15, 2016
Published online: November 28, 2016
Positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) is a diagnostic tool to evaluate metabolic activity by measuring accumulation of FDG, an analogue of glucose, and has been widely used for detecting small tumors, monitoring treatment response and predicting patients’ prognosis in a variety of cancers. However, the molecular mechanism of FDG accumulation into tumors remains to be investigated. It is well-known that most cancers are metabolically active with elevated glucose metabolism, a phenomenon known as the Warburg effect. The underlying mechanisms for elevated glucose metabolism in cancer tissues are complex. Recent reports have indicated the potential of FDG-PET/CT scans in predicting mutational status (e.g., KRAS gene mutation) of colorectal cancer (CRC), which suggests that FDG-PET/CT scans may play a key role in determining therapeutic strategies by non-invasively predicting treatment response to anti-epidermal growth factor receptor (EGFR) therapy. In this review, we summarize the current findings investigating the molecular mechanism of 18F-FDG accumulation in CRC.
Core tip: Malignant cancers are preferential to metabolize glucose by glycolysis, even in the presence of oxygen, so-called Warburg effect. This elevated glucose metabolism is responsible for 18F-fluorodeoxyglucose (FDG) accumulation into cancer cells, which results in the positive signals in FDG-positron emission tomography scans. In spite of its clinical utility, the cellular and molecular mechanisms of 18F-FDG accumulation have not yet been elucidated. Here we review the current literature published with respect to the mechanisms of 18F-FDG accumulation into colorectal cancer tissues.