Figure 10. [11C] and [18F]-ACETATE

In addition to increased glycolytic activity, several alterations of lipid metabolism are often found in cancer cells, including overexpression of fatty acid synthase (FAS).

HER2 signaling has also been implicated as a cause of increased FAS expression.
The mechanisms for apoptosis induced by FAS indicate that this apoptosis may be due to accumulation of FAS substrates triggering AMP-activated protein kinase.

FAS catalyzes the de novo synthesis of fatty acids from acetyl-CoA, malonyl-CoA, and nicotinamide adenine dinucleotide phosphate (NADPH). In the liver and adipose tissue, FAS serves to store energy derived from carbohydrate metabolism as triglycerides. In contrast, human cancer cells do not store significant amounts of triglycerides but esterify fatty acids to phospholipids, such as phophatidylcholine.
Fatty acids are activated to acyl-CoA and in a 2-step reaction form diacylglycerides with glycerol 3-phosphate. These diacylglycerides then react with CDP-choline to form phosphatidylcholine