The Basic Science of 18F-FDG

The role of 18F-FDG in oncology is based on the fact that most cancer cells contain increased intracellular glucose (increased glucose metabolism).

The cellular mechanisms responsible for this phenomenon include:

• Increased vascular tumor blood flow (bringing more glucose to the tumor cells) [Fig. 1]
• Increased expression of tumor cell surface glucose transporters (bringing more glucose into the tumor cells); [Fig. 2] and
• Increased intracellular phosphorylation of glucose (increased trapping of this glucose within the tumor cells). [Fig. 3]

Theory Behind PET Scan Imaging:

We exploit the fact that cancer cells demonstrate increased intracellular glucose. If we can create a radioactive glucose analog, we can label these glucose-filled cancer cells.

In the case of oncologic imaging, 18F-FDG is the most commonly utilized glucose analog.

It is created by the substitution of a positron-emitting radioactive isotope for a hydroxyl group. Though discovered only serendipitously during early neuroimaging research, 18F-FDG’s preferential accumulation in most cancers has rapidly made it a powerful tool in oncologic radiology.

18F-FDG’s long half-life (110 minutes), its ease of incorporation into the glucose molecule, and its low positron energy (permitting higher resolution imaging) make it an ideal oncologic radiotracer.