Metabolism and cancer are closely linked, with cancer cells altering their metabolic pathways to support growth and survival. The Warburg effect, where cancer cells preferentially use glycolysis even in the presence of oxygen, is a key feature of cancer metabolism. This process, along with glutamine, provides carbon skeletons, NADPH, and ATP for new cell formation. Hypoxia in tumors rewires metabolic pathways, and excessive caloric intake increases cancer risk, while caloric restriction may protect against cancer by reducing oxidative stress. Cancer cells rely on glucose and glutamine for energy and biomass production, with glucose being converted to pyruvate and glutamine entering the TCA cycle. Hypoxia activates HIF-1, which promotes glycolysis and inhibits mitochondrial respiration. The TCA cycle is reprogrammed in hypoxic conditions, with glutamine contributing to lipid synthesis and citrate production. Reductive carboxylation of aKG by IDH allows cancer cells to synthesize lipids from glutamine. Oxidative stress from metabolism generates reactive oxygen species (ROS), which can damage DNA and promote mutations. ROS can stabilize HIF-1, further promoting glycolysis and tumor growth. The balance between PFKFB3 and PFKFB4 determines whether glucose is directed toward glycolysis or the PPP. ROS also influence intracellular signaling, affecting cancer cell responses to metabolic stress. Nutrient sensing and signaling pathways, such as those involving AMPK and mTOR, regulate cell growth and metabolism. Myc, an oncogene, drives cell proliferation by stimulating glycolysis, glutaminolysis, and ribosome biogenesis. Mutations in metabolic enzymes, such as IDH, can lead to tumorigenesis through epigenetic changes. mtDNA mutations may also contribute to cancer by affecting mitochondrial function. Oncogenes and tumor suppressors regulate metabolism, with Myc and HIF-1 playing key roles in promoting glycolysis and tumor growth. Loss of p53 favors glycolysis, while p53 activation enhances mitochondrial respiration. The tumor microenvironment influences cancer metabolism, with hypoxia and nutrient limitations affecting metabolic pathways. Therapeutic opportunities exist in targeting cancer metabolism, such as inhibiting glycolysis or glutaminolysis. Drugs targeting metabolic enzymes, like LDHA and glutaminase, show promise in preclinical studies. Understanding the metabolic differences between normal and cancer cells could lead to new therapeutic strategies.Metabolism and cancer are closely linked, with cancer cells altering their metabolic pathways to support growth and survival. The Warburg effect, where cancer cells preferentially use glycolysis even in the presence of oxygen, is a key feature of cancer metabolism. This process, along with glutamine, provides carbon skeletons, NADPH, and ATP for new cell formation. Hypoxia in tumors rewires metabolic pathways, and excessive caloric intake increases cancer risk, while caloric restriction may protect against cancer by reducing oxidative stress. Cancer cells rely on glucose and glutamine for energy and biomass production, with glucose being converted to pyruvate and glutamine entering the TCA cycle. Hypoxia activates HIF-1, which promotes glycolysis and inhibits mitochondrial respiration. The TCA cycle is reprogrammed in hypoxic conditions, with glutamine contributing to lipid synthesis and citrate production. Reductive carboxylation of aKG by IDH allows cancer cells to synthesize lipids from glutamine. Oxidative stress from metabolism generates reactive oxygen species (ROS), which can damage DNA and promote mutations. ROS can stabilize HIF-1, further promoting glycolysis and tumor growth. The balance between PFKFB3 and PFKFB4 determines whether glucose is directed toward glycolysis or the PPP. ROS also influence intracellular signaling, affecting cancer cell responses to metabolic stress. Nutrient sensing and signaling pathways, such as those involving AMPK and mTOR, regulate cell growth and metabolism. Myc, an oncogene, drives cell proliferation by stimulating glycolysis, glutaminolysis, and ribosome biogenesis. Mutations in metabolic enzymes, such as IDH, can lead to tumorigenesis through epigenetic changes. mtDNA mutations may also contribute to cancer by affecting mitochondrial function. Oncogenes and tumor suppressors regulate metabolism, with Myc and HIF-1 playing key roles in promoting glycolysis and tumor growth. Loss of p53 favors glycolysis, while p53 activation enhances mitochondrial respiration. The tumor microenvironment influences cancer metabolism, with hypoxia and nutrient limitations affecting metabolic pathways. Therapeutic opportunities exist in targeting cancer metabolism, such as inhibiting glycolysis or glutaminolysis. Drugs targeting metabolic enzymes, like LDHA and glutaminase, show promise in preclinical studies. Understanding the metabolic differences between normal and cancer cells could lead to new therapeutic strategies.