A very recent result obtained by means of an in vitro experiment with cancer cultured cells has configured the endoplasmic reticulum as the preferential site for the accumulation of 2-deoxy-2-[18F]fluoro-D-glucose (FDG). Such a result is coherent with cell biochemistry and is made more significant by the fact that reticular accumulation rate of FDG is dependent upon extracellular glucose availability. The objective of the present paper was to confirm this result in vivo, using small animal models of CT26 cancer tissues. Specifically, assuming that the endoplasmic reticulum plays a specific functional role in the framework of a three-compartment model for FDG kinetics, we are able to explain positron emission tomography dynamic data in a more reliable way than by means of a standard Sokoloff two-compartment system. This result is made more solid from a computational viewpoint by means of some identifiability considerations based on a mathematical analysis of the compartmental equations.

The role of the endoplasmic reticulum in in vivo cancer FDG kinetics