Cancer cells have a distinct metabolic advantage over normal, nonproliferating cells. Cancer cells must generate enough energy and synthesize sufficient levels of biomolecules to support their rapid proliferation. One of the primary metabolic changes in cancer cells is the Warburg effect, characterized by increased glycolysis and lactate production regardless of oxygen concentration. Unlike oxidative phosphorylation, which is the primary source of ATP in most normal cells, tumor cells have a comparatively greater capacity to use aerobic glycolysis to generate metabolites that are important for cell growth. In order to support proliferation, cancer cells require large amounts of nucleotides, amino acids, and lipids, all of which are used in the synthesis of biological macromolecules. Cancer cells make these macromolecular building blocks from intermediates of the glycolytic pathway, such as glucose-6-phosphate and ribose-5-phosphate, or via protein and lipid biosynthesis, which are regulated by several pathways including mTOR signaling. Oncogenic signaling pathways such as mTOR directly reprogram core carbon metabolism, leading to greater nutrient uptake and greater macromolecular biosynthesis. Several glucose metabolism enzymes such as hexokinase, LDHA, PKM2 and PDK are direct targets of oncogenic transcription factors such as MYC and HIF-1alpha. In addition to increase in aerobic glycolysis, cancer cells have metabolic dependency on glutamine to fuel anabolic processes. Glutamine is another essential nutrient for cancer and is an abundant amino acid in the serum. Mitochondrial enzyme glutaminase (GLS) catalyze the conversion of glutamine to glutamate as a metabolic intermediate to be channeled into the TCA cycle and its function as a precursor for the TCA cycle anaplerosis. Increased expression of glutaminase in tumor and rapidly growing cells is reported. In this session, I will review the characteristics of cancer cell glucose metabolism and discuss the therapeutic potential of targeting metabolic adaptation of cancer cells.