This presentation will discuss efforts to use mathematical modeling to understand the metabolism of tumors. First I will discuss efforts using computational modeling and metabolomics to understand the structure and function of glucose metabolism in cells. I will focus on a phenotype known as the Warburg Effect. The Warburg Effect (WE) is characterized by the increased metabolism of glucose to lactate. It is a common feature of cancers and proliferative diseases but its functions and differences from normal oxidative metabolism are not completely understood. Next I will focus on a network known as one carbon metabolism that integrates nutritional status from multiple sources including glucose to generate multiple biological outputs including anabolic and redox metabolism. This network provides the substrates for methyl groups that mediate the epigenetic status of cells. I will provide evidence that variation in the basal activity of one carbon metabolism is necessary and sufficient to determine methylation status of key epigenetic marks on histones. This finding provides a link between nutrient status and chromatin biology.