Cancer cells rewire their metabolism to support rapid growth, survival, and adaptation. A central feature is the Warburg effect: even in the presence of oxygen, cancer cells preferentially use glycolysis to convert glucose into lactate rather than fully oxidizing it in mitochondria. This yields less ATP per molecule of glucose but provides metabolic intermediates needed for biosynthesis of nucleotides, lipids, and amino acids.

Mitochondria remain active in most cancers. They generate ATP through oxidative phosphorylation and supply key metabolites such as citrate and aspartate. Cancer cells often increase glutamine uptake and catabolism, using glutamine as a carbon and nitrogen source to refill the tricarboxylic acid cycle and sustain anabolic processes.

Altered metabolism is tightly linked to oncogenic signaling. Mutations in genes such as MYC, KRAS, and PI3K, and loss of tumor suppressors like p53, reprogram pathways controlling glucose uptake, glycolysis, lipid synthesis, and redox balance. Some tumors also harbor mutations in metabolic enzymes such as isocitrate dehydrogenase, succinate dehydrogenase, and fumarate hydratase. These changes can produce oncometabolites that inhibit key regulatory enzymes and reshape gene expression and epigenetics.

The tumor microenvironment shapes metabolism further. Limited nutrients and oxygen create regional differences within tumors, leading to metabolic cooperation and competition between cancer cells, stromal cells, and immune cells. This reprogramming influences immune evasion and therapy resistance.

Understanding cancer metabolism is guiding new treatments, including inhibitors of glycolysis, glutaminase, and mutant metabolic enzymes, as well as dietary and metabolic interventions designed to selectively stress tumor cells.