Warburg effect (oncology)

In oncology, the Warburg effect (/ˈvɑːrbʊərɡ/) is the observation that most cancer use aerobic glycolysis for energy generation rather than the mechanisms used by non-cancerous cells.[1] This observation was first published by Otto Heinrich Warburg,[2] who was awarded the 1931 Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme".[3] The existence of the Warburg effect has fuelled popular misconceptions that cancer can be treated by dietary reductions in sugar and carbohydrate, according to an article in the Lancet.[1]

In fermentation, the last product of glycolysis, pyruvate, is converted into lactate (lactic acid fermentation) or ethanol (alcoholic fermentation). While fermentation produces adenosine triphosphate (ATP) only in low yield compared to the citric acid cycle and oxidative phosphorylation of aerobic respiration, it allows proliferating cells to convert nutrients such as glucose and glutamine more efficiently into biomass by avoiding unnecessary catabolic oxidation of such nutrients into carbon dioxide, preserving carbon-carbon bonds and promoting anabolism.[4][failed verification]

Diagnostically the increased glucose consumption by cancer cells resulting from the Warburg effect is the basis for tumor detection in a PET scan, in which an injected radioactive glucose analog is detected at higher concentrations in malignant cancers than in other tissues.[5]

  1. ^ a b Cite error: The named reference mis was invoked but never defined (see the help page).
  2. ^ Alfarouk KO (December 2016). "Tumor metabolism, cancer cell transporters, and microenvironmental resistance". Journal of Enzyme Inhibition and Medicinal Chemistry. 31 (6): 859–66. doi:10.3109/14756366.2016.1140753. PMID 26864256.
  3. ^ "The Nobel Prize in Physiology or Medicine 1931". Nobel Foundation. Retrieved 20 April 2007.
  4. ^ Vander Heiden MG, Cantley LC, Thompson CB (May 2009). "Understanding the Warburg effect: the metabolic requirements of cell proliferation". Science. 324 (5930): 1029–1033. Bibcode:2009Sci...324.1029V. doi:10.1126/science.1160809. PMC 2849637. PMID 19460998.
  5. ^ Batra S, Adekola KU, Rosen ST, Shanmugam M (May 2013). "Cancer metabolism as a therapeutic target". Oncology. 27 (5). Williston Park, N.Y.: 460–467. PMID 25184270.