Tumor cells exhibit increased metabolic autonomy compared to normal cells, utilizing nutrients and metabolizing them to support growth and proliferation. While classical research focused on bioenergetics, particularly glycolysis and reduced oxidative phosphorylation (the Warburg effect), recent studies highlight the importance of biosynthetic pathways for tumor growth. This review discusses how tumor cells achieve high rates of nucleotide and fatty acid synthesis, the role of oncogenes and tumor suppressors, and how glutamine metabolism supports macromolecular synthesis. Tumor cells generate ribose-5-phosphate (R5P) for nucleotide biosynthesis by diverting glycolytic carbon into the pentose phosphate pathway. p53 influences this process by suppressing glycolysis and enhancing oxidative flux. In p53-deficient cells, PK-M2 expression allows glycolytic intermediates to accumulate, promoting non-oxidative pentose phosphate pathway activity. This pathway is crucial for R5P synthesis and is linked to tumor growth. Tumor cells also synthesize fatty acids and lipids, using glucose as a carbon source and glutamine for nitrogen. Oncogenic mutations, particularly those in the PI3K/Akt/mTOR pathway, enhance fatty acid synthesis by increasing the expression of lipogenic enzymes. These enzymes, including ATP-citrate lyase (ACL), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS), are essential for lipid biosynthesis. However, fatty acid synthesis requires anaplerosis and NADPH production, which are supported by glutamine metabolism. Glutamine metabolism provides both anaplerotic and NADPH demands for tumor cell growth. Glutaminolysis, the metabolism of glutamine to lactate, is a hallmark of tumor cell metabolism. This process generates NADPH for fatty acid synthesis and provides carbon for the TCA cycle. Glutamine-derived carbon and nitrogen are secreted as lactate and alanine, which can be used for hepatic gluconeogenesis, providing more fuel for tumor metabolism. In conclusion, enhanced biosynthetic capacity is a key feature of tumor cell metabolism. The synthesis of nucleotides and fatty acids, along with the consumption of glucose and glutamine, is prevalent in tumors. Understanding how these activities are regulated in tumor cells, including their relationship to the cell cycle, remains an important area of research. The role of glutamine metabolism in supporting biosynthetic activities highlights the complexity of tumor cell metabolism and its potential as a therapeutic target.Tumor cells exhibit increased metabolic autonomy compared to normal cells, utilizing nutrients and metabolizing them to support growth and proliferation. While classical research focused on bioenergetics, particularly glycolysis and reduced oxidative phosphorylation (the Warburg effect), recent studies highlight the importance of biosynthetic pathways for tumor growth. This review discusses how tumor cells achieve high rates of nucleotide and fatty acid synthesis, the role of oncogenes and tumor suppressors, and how glutamine metabolism supports macromolecular synthesis. Tumor cells generate ribose-5-phosphate (R5P) for nucleotide biosynthesis by diverting glycolytic carbon into the pentose phosphate pathway. p53 influences this process by suppressing glycolysis and enhancing oxidative flux. In p53-deficient cells, PK-M2 expression allows glycolytic intermediates to accumulate, promoting non-oxidative pentose phosphate pathway activity. This pathway is crucial for R5P synthesis and is linked to tumor growth. Tumor cells also synthesize fatty acids and lipids, using glucose as a carbon source and glutamine for nitrogen. Oncogenic mutations, particularly those in the PI3K/Akt/mTOR pathway, enhance fatty acid synthesis by increasing the expression of lipogenic enzymes. These enzymes, including ATP-citrate lyase (ACL), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS), are essential for lipid biosynthesis. However, fatty acid synthesis requires anaplerosis and NADPH production, which are supported by glutamine metabolism. Glutamine metabolism provides both anaplerotic and NADPH demands for tumor cell growth. Glutaminolysis, the metabolism of glutamine to lactate, is a hallmark of tumor cell metabolism. This process generates NADPH for fatty acid synthesis and provides carbon for the TCA cycle. Glutamine-derived carbon and nitrogen are secreted as lactate and alanine, which can be used for hepatic gluconeogenesis, providing more fuel for tumor metabolism. In conclusion, enhanced biosynthetic capacity is a key feature of tumor cell metabolism. The synthesis of nucleotides and fatty acids, along with the consumption of glucose and glutamine, is prevalent in tumors. Understanding how these activities are regulated in tumor cells, including their relationship to the cell cycle, remains an important area of research. The role of glutamine metabolism in supporting biosynthetic activities highlights the complexity of tumor cell metabolism and its potential as a therapeutic target.