The major biosynthetic activities used by proliferating tumor cells (synthesis of proteins, nucleic acids and lipids) are outlined in boxes. Supporting pathways, including glycolysis, the oxidative and non-oxidative arms of the pentose phosphate pathway, mitochondrial glutamine metabolism and the TCA cycle are also shown. Alternative metabolic pathways normally used during nutrient deprivation and suppressed during cell proliferation (β-oxidation of fatty acids, autophagy) are indicated by dashed lines. Selected effects of p53, Myc, Ras and the PI3K/Akt/mTOR signaling system (boxed P) are indicated; black symbols indicate supression and white symbols indicate activation. In the case of p53, loss of function mutations in tumor cells have the opposite of the effect shown here (e.g. glucose uptake and glycolysis are no longer suppressed by p53 activity). Abbreviations: Glc, glucose; G6P, glucose-6-phosphate; F6P, fructose-6-phosphate; F1,6biP, fructose-1,6-bisphosphate; F2,6biP, fructose-2,6-bisphosphate; GA3P, glyceraldehyde 3-phosphate; Pyr, pyruvate; Lac, lactate; R5P, ribose-5-phosphate; PRPP, 5-phosphoribosyl pyrophosphate; Ser, serine; Gly, glycine; Ac-CoA, acetyl-CoA; Cit, citrate; α-KG, α-ketoglutarate; Succ, succinate; OAA, oxaloacetate; Mal-CoA, malonyl-CoA; Gln, glutamine; Glu, glutamate, NH4+, ammonia; TIGAR, TP53-induced glycolysis and apoptosis regulator; PFK1, phosphofructokinase-1; PGAM, phosphoglycerate mutase; SHMT, serine hydroxymethyltransferase.