Potential role of FDG-PET imaging in understanding tumor-host interaction

Population ecology mathematical models of tumorigenesis have been developed to define the cellular characteristics which allow a transformed population to begin as a single individual but end with complete destruction of the host. To invade and expand, a tumor population must compete successfully with normal cells for space and critical, shared substrate such as glucose. This study uses population ecology models to examine the potential role of competition for glucose in tumor biology and its implications for FDG-PET imaging.

Chemostat population ecology mathematical models of the tumor-host interface are developed resulting in coupled, nonlinear differential equations which link population growth to acquisition and utilization of glucose.

The models demonstrate that increased FDG uptake in tumors observed on PET imaging is the result of increased consumption necessary to provide surplus energy for reproduction when inefficient glycolytic pathways are used for glucose metabolism. Specific parameters of the glucose consumption curves are predicted to be markedly different in normal and neoplastic tissues and critical to the tumor-host interaction. Tumor invasability and patient prognosis can be linked to these parameters.

The mathematical models link FDG-PET imaging with processes fundamental to the outcome of the tumor host interaction. The value of FDG-PET can be expanded by quantitation of glucose uptake parameters which will be highly specific in tumor detection and strong indicators of tumor aggressiveness. Therapeutic modalities designed to decrease tumor glucose uptake or increase glucose uptake in normal tissue could be directed and monitored by FDG-PET.