**3. Fluorodeoxyglucose**

#### **3.1. Tumour detection**

F-18 FDG is an analogue of glucose (**Figure 1**). Its active transport into the cell is mediated by a group of structurally related glucose transport proteins (GLUT) and once intracellular, FDG

**Figure 1.** Chemical structure of F-18 fluorodeoxyglucose.

is phosphorylated by the enzyme hexokinase as the first step towards glycolysis. However, unlike glucose, once phosphorylated FDG-6-phosphate cannot continue along the glycolytic pathway and effectively becomes trapped intracellularly. FDG uptake in PET is thus an indication of the metabolic activity of the structure in which it is being taken up. Most malignant cells are metabolically active and demonstrate an increased expression of glucose transport proteins, particularly GLUT-1 and GLUT-3, as well as higher levels of hexokinase.

FDG is the single most important, widely used and explored radiotracer in PET; however, its current role in brain tumour imaging is limited due to the presence of intense physiological FDG uptake in the normal brain resulting in poor tumour-to-background contrast. Thus, an underlying brain tumour, even if FDG-avid, can escape detection on FDG PET (**Figure 2**). In some studies, increased FDG uptake in gliomas was only reported in 21–47% of high-grade tumours and as few as 3–6% of low-grade tumours [4, 5]. Delayed imaging (e.g. 6 h) follow‐ ing FDG administration instead of the usual imaging performed 60–90 min post-radiotracer can improve discrimination between tumour and physiological background uptake as FDG is retained in tumour longer than in normal brain parenchyma [6].

**Figure 2.** FDG uptake in a left frontal cerebral glioma on PET/CT. *Top row:* The tumour is not readily discernible from intense physiological FDG activity in the adjacent cerebral parenchyma. *Bottom row:* The tumour is much better depict‐ ed on MRI FLAIR imaging (*bottom left panel*) and shows no contrast enhancement due to its low grade (*bottom right panel*).
