Tumor metabolism refers to the altered ways cancer cells obtain and use energy and building blocks to support uncontrolled growth, survival and spread. A central feature is the Warburg effect: many tumor cells take up large amounts of glucose and favor glycolysis followed by lactate production, even when oxygen is available. This aerobic glycolysis is less efficient for ATP generation but rapidly provides intermediates for biosynthesis and can help tumors adapt to fluctuating oxygen and nutrient levels.

Oncogenes and tumor suppressor genes rewire metabolism. Mutations in signaling pathways such as PI3K, AKT and mTOR increase glucose uptake, glycolytic flux and lipid synthesis. Loss of p53 can reduce oxidative phosphorylation and antioxidant defense control. Some tumors depend on glutamine as a key carbon and nitrogen source for the tricarboxylic acid cycle, nucleotide production and redox balance. Others rely on fatty acid synthesis or oxidation, or scavenge lipids from their environment.

The tumor microenvironment shapes metabolic behavior. Poor blood supply causes hypoxia and low nutrient availability, activating HIF transcription factors and stress pathways that further promote glycolysis, angiogenesis and metabolic flexibility. Cancer cells compete with immune cells for nutrients and can secrete metabolites such as lactate that acidify the microenvironment and suppress antitumor immunity.

These insights are driving new therapeutic strategies. Approaches under study include targeting specific metabolic enzymes and transporters, exploiting synthetic lethal interactions, restricting nutrients or metabolic pathways that tumors depend on, and combining metabolic drugs with immunotherapies or conventional treatments to improve efficacy and limit resistance.