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)
Show evidence (1 reference)
"A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass."
Establishes deregulated nutrient acquisition as a common feature of cancer metabolism, the trigger of this module. Evidence source is OTHER because this is a review article.
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
Show evidence (2 references)
"most cancer cells produce large amounts of lactate regardless of the availability of oxygen"
Directly describes aerobic glycolysis (lactate production despite adequate oxygen), the central effector of this module. Evidence source is OTHER because this is a review article.
"reprogramming of energy metabolism and evading immune destruction"
Hanahan & Weinberg name reprogramming of energy metabolism as an emerging hallmark, the capability modeled here. Evidence source is OTHER because this is a review article.
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.
Show evidence (1 reference)
"most cancer cells instead rely on aerobic glycolysis"
Supports the reliance on aerobic glycolysis whose biosynthetic role (channeling nutrients into biomass) is modeled in this consequence node. Evidence source is OTHER because this is a review article.