Population ecology mathematical models of tumorigenesis have been deve
loped to define the cellular characteristics which allow a transformed
population to begin as a single individual but end with complete dest
ruction of the host. To invade and expand, a tumor population must com
pete successfully with normal cells for space and critical, shared sub
strate such as glucose. This study uses population ecology models to e
xamine the potential role of competition for glucose in tumor biology
and its implications for FDG-PET imaging. Methods: Chemostat populatio
n ecology mathematical models of the tumor-host interface are develope
d resulting in coupled, nonlinear differential equations which link po
pulation growth to acquisition and utilization of glucose. Results: Th
e models demonstrate that increased FDG uptake in tumors observed on P
ET 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 co
nsumption curves are predicted to be markedly different in normal and
neoplastic tissues and critical to the tumor-host interaction. Tumor i
nvasability and patient prognosis can be linked to these parameters. C
onclusion: The mathematical models link FDG-PET imaging with processes
fundamental to the outcome of the tumor host interaction. The value o
f FDG-PFT can be expanded by quantitation of glucose uptake parameters
which will be highly specific in tumor detection and strong indicator
s of tumor aggressiveness. Therapeutic modalities designed to decrease
tumor glucose uptake or increase glucose uptake in normal tissue coul
d be directed and monitored by FDG-PET.