Towards an integrative model of the PI3K/Akt metabolic effects

Cancer cells differ from their normal counterparts more in terms of regulatory networks than of specific molecules. A recently recognized hallmark of cancer is the increased uptake of nutrients, particularly glucose, associated with a higher lactate pro- duction. A common step of tumorigenesis, which influences these metabolic alterations, is the constitutive activation of phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Fol- lowing an integrative systems biology approach, we propose a model for the in silico investigation of the PI3K/Akt pathway effects on the central metabolism. This model represents a useful tool for the computational analysis of the metabolic differences be- tween normal and pathological conditions.