This is a mechanism module, not a specific disease. Disorder entries reference individual nodes via conforms_to (e.g., "deregulated_cellular_energetics#Aerobic Glycolysis (Warburg Effect)"). The module defines the expected pathophysiology structure; conforming nodes in disorder files should include the corresponding biological processes and causal edges, specialized to their tumor context. Key tumor-specific substitutions: MYC/PI3K-AKT-driven tumors show glucose and glutamine addiction; IDH-mutant gliomas/AML produce the oncometabolite 2-hydroxyglutarate that reprograms the epigenome; VHL-deficient renal cell carcinoma uses HIF-driven glycolysis. Key conformance target: "deregulated_cellular_energetics#Aerobic Glycolysis (Warburg Effect)".
Oncogene-Driven Nutrient Uptake
trigger
Normal cells take up nutrients only when stimulated by growth factors; cancer cells acquire mutations that constitutively activate nutrient-uptake and metabolic signaling (PI3K-AKT-mTOR, MYC, RAS), upregulating glucose transporters (GLUT1) and amino-acid transporters. This cell-autonomous, growth-factor-independent nutrient acquisition is the metabolic entry point of the hallmark.
Downstream
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Aerobic Glycolysis (Warburg Effect)
Aerobic Glycolysis (Warburg Effect)
central effector
Cancer cells preferentially metabolize glucose to lactate even in the presence of oxygen sufficient for oxidative phosphorylation - the Warburg effect. Though inefficient in ATP yield per glucose, high glycolytic flux rapidly regenerates ATP and, critically, supplies carbon intermediates for biosynthesis. This is the conserved central node of the metabolic hallmark; it does not require defective mitochondria.
Downstream
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Biosynthetic Diversion for Biomass Production
Biosynthetic Diversion for Biomass Production
consequence
Glycolytic and TCA-cycle intermediates are diverted into anabolic pathways: glucose-6-phosphate into the pentose phosphate pathway for ribose and NADPH, 3-phosphoglycerate into serine/glycine and one-carbon metabolism, citrate into fatty-acid synthesis, and glutamine into anaplerosis and nitrogen for nucleotide/amino-acid synthesis. This diversion converts nutrients into the macromolecular building blocks (nucleotides, amino acids, lipids) required to produce a new cell, the biosynthetic purpose of the Warburg phenotype.