Tumor metabolism research focuses on how cancer cells alter energy and nutrient use to support uncontrolled growth, survival and spread. A central concept is metabolic reprogramming. Cancer cells often increase glucose uptake and rely heavily on glycolysis, even when oxygen is available, a phenomenon known as the Warburg effect. This provides rapid ATP and biosynthetic precursors while producing lactate, which acidifies the tumor microenvironment and promotes invasion, immune evasion and angiogenesis.

Beyond glucose, tumors rewire amino acid and lipid metabolism. Many cancers become dependent on glutamine for energy, nucleotide synthesis and maintenance of redox balance. Others show heightened serine and glycine metabolism to support one carbon pathways critical for DNA synthesis and methylation. Fatty acid synthesis and oxidation are frequently upregulated, supplying membranes, signaling molecules and additional energy.

The tumor microenvironment plays a key role. Limited oxygen and nutrients, along with interactions with stromal and immune cells, further shape metabolic pathways. Cancer associated fibroblasts, endothelial cells and immune cells can exchange metabolites with tumor cells, establishing a cooperative and competitive metabolic network. This environment also influences immune cell function, often suppressing effective antitumor responses through nutrient depletion and accumulation of immunosuppressive metabolites such as adenosine and kynurenine.

Therapeutically, these metabolic peculiarities create vulnerabilities. Inhibitors of glycolysis, glutaminase, lipid biosynthesis and key nodes in one carbon metabolism are under investigation. Combining metabolic drugs with targeted therapies, chemotherapy, radiotherapy or immunotherapy aims to enhance treatment efficacy and overcome resistance by cutting off the metabolic support systems that cancer cells rely on.