Tumours frequently reprogram multiple pathways involved in nutrient acquisition and metabolism to meet their demands in bioenergetic, biosynthetic, and redox activities. These reprogrammed activities are now recognised as a general hallmark of cancer. Although mitochondrial dysfunction is observed in some cancers, most cancers maintain functional mitochondria but with altered/rewired mitochondrial metabolism. In cancer cells the tricarboxylic acid (TCA) cycle is often rewired to support biosynthesis, providing intermediates for nucleotide, amino acid, and lipid synthesis. This use of aerobic glycolysis in cancer cells (the Warburg effect) provided the original example of a reprogrammed metabolic pathway in cancer. In normal tissues glycolysis is engaged as a physiological response to hypoxia, but Otto Warburg in the 1920s observed that tumours constitutively utilize glucose regardless of oxygen availability to produce lactate, an observation that has been subsequently replicated in many types of tumours. The increase in glycolytic flux allows glycolytic intermediates to supply subsidiary pathways that meet the increased metabolic demands of proliferating cells under conditions where nutrients may be limiting. Like glycolytic intermediates, TCA cycle intermediates are also used as precursors for biosynthesis. The pentose phosphate pathway (PPP, also known as the phosphogluconate pathway or the hexose monophosphate shunt), is a metabolic pathway parallel to glycolysis, and represents the first committed step in glucose metabolism. The PPP supports tumour cell survival and growth by generating pentose phosphate (used for nucleic acid synthesis) and providing nicotinamide-adenine dinucleotide phosphate (NADPH), which is needed for fatty acid synthesis and for cell survival under redox stress conditions. Previous studies indicate that PPP flux is directly or indirectly modulated in cancer cells, thereby increasing cell survival and proliferation. Therefore, the regulatory network of PPP flux is important for cancer cell metabolism. Cancer cells also have an increased demand for nutrient amino acids to support protein synthesis and cellular growth and acquire them through a variety of mechanisms including increased uptake or de novo synthesis. Certain amino acids, such as glutamine, serine, glycine, and cysteine play particularly important and distinct roles in cancer metabolism. Cancer cells also require lipids for membrane synthesis, energy storage, and cell signalling and often exhibit alterations in lipid metabolism, including increased fatty acid synthesis, enhanced lipid uptake, and changes in lipid composition. Cancer cells also exhibit higher levels of oxidative stress than normal cells due to increased metabolic activity associated with rapid proliferation and mitochondrial dysfunction. They frequently maintain redox balance by upregulating antioxidant defence systems, such as glutathione and thioredoxin pathways to counteract oxidative damage. Finally, cancer cells often exhibit metabolic plasticity, allowing them to adapt to different nutrient and oxygen availabilities, switching between different metabolic pathways based on the availability of nutrients and the energy demands of proliferation. Metabolic heterogeneity can also exist within a single tumour, with different subclones utilizing different metabolic pathways. We provide a comprehensive product range of research tools for studying cellular metabolic processes, including Bcl-2 antibodies, Myeloperoxidase antibodies, NCF1 antibodies, Myeloperoxidase ELISA Kits, and Glutathione Peroxidase 1 ELISA Kits. Explore our full cellular metabolic process product range below and discover more, for less.