The Warburg Effect and Aerobic Glycolysis in Tumors.
Level 5 - mechanism / opinion, no new human data
Narrative review and book chapter describing mechanistic pathways without original human data
PubMed 42144518 · doi:10.1007/978-3-032-21861-2_2
What was done
This narrative review and book chapter synthesizes the biochemical, molecular, and physiological dimensions of aerobic glycolysis (the Warburg effect) in tumors, examining its mechanistic regulation by oncogenes, tumor suppressors, and transcriptional networks, as well as therapeutic approaches targeting cancer metabolism.
What was found
The abstract reports no empirical numbers or quantitative findings. It describes qualitatively that aerobic glycolysis facilitates macromolecular synthesis through intermediate accumulation, maintains redox homeostasis via NADPH generation, and promotes invasion and immune evasion through extracellular microenvironment acidification, regulated by factors including MYC, RAS, PI3K, p53, LKB1, and HIF-1α.
Why it matters
The review outlines how tumor glycolytic dependency intersects with cellular signaling and stromal interactions, highlighting potential metabolic targets for cancer therapy.
Limits
This is a narrative overview and book chapter with no original primary data, systematic search methodology, or quantitative effect estimates. No clinical trials or patient-level outcomes are evaluated.
Cited by
- supports Cancer cells exhibit the Warburg effect by opting for fermentation and avoiding mitochondrial respiration even in the presence of oxygen.