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Tumor metabolic pathway refers to the spectrum of metabolic processes that are rewired or dysregulated in cancer cells to support their enhanced needs for energy, biosynthesis, and survival. This concept encompasses changes to carbohydrate metabolism (such as increased glycolysis, known as the Warburg effect), amino acid metabolism, lipid metabolism, nucleotide synthesis, and redox homeostasis. Different cancers, and even subtypes within the same cancer, display distinct patterns of metabolic reprogramming, often controlled by oncogenic mutations (e.g., MYC, TP53, IDH1/2) and signaling pathways (e.g., mTORC1). These features are central to tumor pathophysiology, influence patient prognosis, and provide potential—but complex—therapeutic opportunities[1][3]. There is no single molecular target or canonical "tumor metabolic pathway" protein; instead, this term captures a large set of dynamic and intersecting metabolic adaptations characteristic of malignant cells[1][3].
Mechanisms are pathway- and enzyme-specific, e.g., inhibition of isocitrate dehydrogenase, PI3K/AKT/mTOR signaling modulation, glycolytic inhibition. Specific drugs do not directly target "tumor metabolic pathway" as a whole, but rather individual enzymes or nodes within specific pathways such as glycolysis, glutaminolysis, or the TCA cycle; examples include inhibitors of IDH1, IDH2, or metabolic checkpoints like mTOR.
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