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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
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Fuel Economy for Growing Cells: Sophisticated 21st-century analyses of the signaling pathways that control cell growth have led researchers back to the seminal work of Otto Warburg, who discovered in the 1920s that tumor cells generate their energy in an unusual way—by switching from mitochondrial respiration to glycolysis. The advantage conferred by this metabolic switch is puzzling because mitochondrial respiration is a more efficient way to produce ATP. Vander Heiden et al. (p. 1029 ) review arguments that rapidly growing cells have critical metabolic requirements that extend beyond ATP and that a better understanding of these requirements may shed new light on the “Warburg effect” and ultimately lead to new therapies for cancer.
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In the paper
“This 35-fold asymmetry is only partially compensated by the consumption of 3 glucose molecules in acetyl-CoA production to satisfy the carbon requirement of the acyl chain itself.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
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In the paper
“Some glucose must be diverted to macromolecular precursors such as acetyl-CoA for fatty acids, glycolytic intermediates for nonessential amino acids, and ribose for nucleotides.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Inhibiting LDH activity impairs cell proliferation (6)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [6] Fantin VR St-Pierre J Leder P Cancer Cell 9 425 2006 16766262
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In the paper
“Most of the carbon for fatty acid synthesis is derived from glucose.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
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In the paper
“Normal proliferating cells can also undergo cell cycle arrest and reactivate catabolic metabolism when their ability to produce ATP from glucose is compromised (12, 13)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Why Do Proliferating Cells Switch to a Less Efficient Metabolism?
What the sources say
- Not checked yetcites [12] Shaw RJ Proc Natl Acad Sci USA 101 3329 2004 14985505 PMC373461
- Not checked yetcites [13] Lum JJ Cell 120 237 2005 15680329
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In the paper
“subsequent work showed that mitochondrial function is not impaired in most cancer cells (5–7)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Proliferating Mammalian Cells Exhibit Anabolic Metabolism
What the sources say
- Not checked yetcites [5] Weinhouse S Z Krebsforsch Klin Onkol Cancer Res Clin Oncol 87 115 1976 136820
- Not checked yetcites [6] Fantin VR St-Pierre J Leder P Cancer Cell 9 425 2006 16766262
- Not checked yetcites [7] Moreno-Sanchez R Rodriguez-Enriquez S Marin-Hernandez A Saavedra E FEBS J 274 1393 2007 17302740
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“This may explain at least part of the selective advantage provided by the Warburg effect”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [16] DeBerardinis RJ Proc Natl Acad Sci USA 104 19345 2007 18032601 PMC2148292
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In the paper
“To produce two viable daughter cells at mitosis, a proliferating cell must replicate all of its cellular contents. This imposes a large requirement for nucleotides, amino acids, and lipids.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
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In the paper
“even minor perturbations in the ATP/ADP ratio can impair growth”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Why Do Proliferating Cells Switch to a Less Efficient Metabolism?
What the sources say
- Not checked yetcites [10] Izyumov DS Biochim Biophys Acta 1658 141 2004 15282185
- Not checked yetcites [11] Vander Heiden MG Chandel NS Schumacker PT Thompson CB Mol Cell 3 159 1999 10078199
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In the paper
“glucose and glutamine supply most of the carbon, nitrogen, free energy, and reducing equivalents necessary to support cell growth and division”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: For most mammalian cells in culture, glucose and glutamine are the only two molecules catabolized in appreciable quantities.
- It may state two separate claims as one. 19
- Probably not a substantial claim. 6
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In the paper
“to make a 16-carbon fatty acyl chain, a single glucose molecule can provide five times the ATP required, whereas 7 glucose molecules are needed to generate the NADPH required”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
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In the paper
“synthesis of palmitate, a major constituent of cellular membranes, requires 7 molecules of ATP, 16 carbons from 8 molecules of acetyl-CoA (coenzyme A), and 28 electrons from 14 molecules of NADPH”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [8] Lehninger AL Nelson DL Cox MM Principles of Biochemistry Worth New York 2 1993
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In the paper
“Synthesis of acetyl-CoA from citrate requires the enzyme ATP citrate lyase (ACL), and disruption of ACL impairs tumor growth (18).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [18] Hatzivassiliou G Cancer Cell 8 311 2005 16226706
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A second possible explanation for the switch to aerobic glycolysis, discussed in detail below, is that proliferating cells have important metabolic requirements that extend beyond ATP.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Why Do Proliferating Cells Switch to a Less Efficient Metabolism?
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In the paper
“Growth factor signaling also regulates the activity of the glycolytic enzyme pyruvate kinase and modulates flux of carbon through the later steps of glycolysis (9, 17).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [9] Christofk HR Nature 452 230 2008 18337823
- Not checked yetcites [17] Christofk HR Vander Heiden MG Wu N Asara JM Cantley LC Nature 452 181 2008 18337815
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In the paper
“A glucose molecule can generate up to 36 ATPs, or 30 ATPs and 2 NADPHs [if diverted into the pentose phosphate shunt (8, 15)], or provide 6 carbons for macromolecular synthesis.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [8] Lehninger AL Nelson DL Cox MM Principles of Biochemistry Worth New York 2 1993
- Not checked yetcites [15] Possibly up to four NADPH molecules per glucose can be produced if the products of the pentose phosphate shunt are metabolized via the TCA cycle and malic enzyme or cytosolic isocitrate dehydrogenase 1 (IDH1) to generate two additional NADPH molecules.
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In the paper
“The metabolism of glucose to lactate generates only 2 ATPs per molecule of glucose, whereas oxidative phosphorylation generates up to 36 ATPs upon complete oxidation of one glucose molecule (8).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Why Do Proliferating Cells Switch to a Less Efficient Metabolism?
What the sources say
- Not checked yetcites [8] Lehninger AL Nelson DL Cox MM Principles of Biochemistry Worth New York 2 1993
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In the paper
“Glucose withdrawal induces cell death in a manner indistinguishable from that seen upon withdrawal of growth factor signaling, a phenomenon that may contribute to “oncogene addiction” (22).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
What the sources say
- Not checked yetcites [22] Vander Heiden MG Mol Cell Biol 21 5899 2001 11486029 PMC87309
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In the paper
“PI3K signaling through AKT can regulate glucose transporter expression, enhance glucose capture by hexokinase, and stimulate phosphofructokinase activity (2)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
What the sources say
- Not checked yetcites [2] Deberardinis RJ Lum JJ Hatzivassiliou G Thompson CB Cell Metab 7 11 2008 18177721
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In the paper
“Small molecules that disrupt PI3K signaling lead to decreased glucose uptake by tumors as measured by 18F-deoxyglucose positron emission tomography (FDG-PET), and the ability to inhibit tumor FDG uptake correlates with tumor regression (21).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
What the sources say
- Not checked yetcites [21] Engelman JA Nat Med 14 1351 2008 19029981 PMC2683415
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In the paper
“p53 expression controls metabolic genes and alters glucose utilization”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Expression of TIGAR, a gene induced by p53, leads to inhibition of phosphofructokinase, redirection of glucose toward the pentose phosphate shunt, and NADPH production (34).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
What the sources say
- Not checked yetcites [34] Bensaad K Cell 126 107 2006 16839880
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Possibly the dumping of excess carbon as lactate is effective because it allows faster incorporation of carbon into biomass, which in turn facilitates rapid cell division.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“oncogenic Ras causes alterations in glucose metabolism (35) but causes senescence when expressed in cells without a cooperating oncogene (36)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
What the sources say
- Not checked yetcites [35] Chiaradonna F Oncogene 25 5391 2006 16607279
- Not checked yetcites [36] Serrano M Lin AW McCurrach ME Beach D Lowe SW Cell 88 593 1997 9054499
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In the paper
“The Cori cycle in the liver can recycle lactate generated from actively proliferating tissues to glucose, and analogous pathways exist to recycle the alanine generated from “inefficient” glutamine metabolism (8).”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Crunching the Numbers–What Are the Metabolic Needs of Proliferating Cells?
What the sources say
- Not checked yetcites [8] Lehninger AL Nelson DL Cox MM Principles of Biochemistry Worth New York 2 1993
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“IDH1 and IDH2 couple the interconversion of cytosolic isocitrate and α-ketoglutarate in an NADP+/NADPH-dependent reaction.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
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In the paper
“Mitochondrial oxidative phosphorylation is the major cellular source of ROS production.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Metabolic Regulation Is a Component of the Cell Growth Machinery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
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In the paper
“leukemic cells are highly glycolytic (40, 41), yet these cells reside within the bloodstream at higher oxygen tensions than cells in most normal tissues”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > What Triggers the Switch from Oxidative Phosphorylation to Aerobic Glycolysis?
What the sources say
- Not checked yetcites [40] Gottschalk S Anderson N Hainz C Eckhardt SG Serkova NJ Clin Cancer Res 10 6661 2004 15475456
- Not checked yetcites [41] Elstrom RL Cancer Res 64 3892 2004 15172999
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Perhaps one function of oncogenic pathways is to drive cell-autonomous nutrient uptake and program proliferative metabolism, whereas one function of tumor suppressor pathways is to prevent nutrient utilization for anabolic processes.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > What Triggers the Switch from Oxidative Phosphorylation to Aerobic Glycolysis?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the available evidence suggests that it is a late-occurring event that may not be a major contributor in the switch to aerobic glycolysis by cancer cells”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > What Triggers the Switch from Oxidative Phosphorylation to Aerobic Glycolysis?
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“There is mounting evidence for cross-talk between signaling pathways and metabolic control in every multicellular organism studied.”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Future Prospects
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In the paper
“Metformin and the more potent related compound Phenformin activate AMPK in cells”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Cellular Metabolism and Human Cancer
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In the paper
“the widely used diabetes drug metformin may offer a possible benefit in cancer prevention as well as improved outcomes when used with other cancer therapies (44)”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Cellular Metabolism and Human Cancer
What the sources say
- Not checked yetcites [44] Evans JM Donnelly LA Emslie-Smith AM Alessi DR Morris AD BMJ 330 1304 2005 15849206 PMC558205
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“a large fraction of human cancer is dependent on aberrant signaling through the PI3K/Akt pathway”
§ Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation > Cellular Metabolism and Human Cancer
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper relies on this without support.
For most mammalian cells in culture, glucose and glutamine are the only two molecules catabolized in appreciable quantities.
“For most mammalian cells in culture, the only two molecules catabolized in appreciable quantities are glucose and glutamine.”
The paper relies on this without support.
Nutrients are not limiting for most proliferating cells.
“For most proliferating cells, nutrients are not limiting so there is no selective pressure to optimize metabolism for ATP yield.”
Claims other papers make about this one
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In the citing paper
“high levels of ROS generated by ongoing aerobic glycolysis followed by pyruvate oxidation in mitochondria (the Warburg effect), increase receptor and oncogene activity, and the stimulation of growth factor-dependent pathways or oxidizing enzymes induce genetic instability3,4.”
From ROS in cancer therapy: the bright side of the moon (2020) · cites this paper as [3]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“As a result, the metabolic phenotype of immortalized cell lines may diverge from the native metabolic profile of their tissue of origin (Vander Heiden et al. 2009;Liberti and Locasale 2016).”
From Primary cell cultures versus immortalized cell lines: critical comparative insights into biological fidelity and translational applications (2026) · cites this paper as Vander Heiden et al. 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Moreover, the augmentation of aerobic glycolysis could aid in the mitigation of reactive oxygen species and additionally facilitate the production of a greater quantity of amino acids to support protein synthesis in osteoblasts [58].”
From Mesenchymal stromal cells in bone marrow niche of patients with multiple myeloma: a double-edged sword (2025) · cites this paper as [58]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The ATP that is necessary for fungal cell growth and function is synthesized mainly through oxidative phosphorylation (OXPHOS), with the key enzyme being F1Fo-ATP synthase4.”
From The δ subunit of F1Fo-ATP synthase is required for pathogenicity of Candida albicans (2021) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“PI3K signaling may be central to linking the common genetic perturbations of cancer, such as RTK mutations and PTEN loss, with altered metabolic processes, including the “lipogenic phenotype” common to many cancers, including GBM (13, 14, 17, 20).”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [17]
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“This metabolic reprogramming supports rapid and sustained proliferation by generating ATP, maintaining redox homeostasis, and diverting glycolytic intermediates into biosynthetic pathways required for macromolecular synthesis (Vander Heiden et al. 2009;Liberti and Locasale 2016).”
From Primary cell cultures versus immortalized cell lines: critical comparative insights into biological fidelity and translational applications (2026) · cites this paper as Vander Heiden et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“In addition to these transcriptional and epigenetic concerns, CR may also influence the underlying metabolic state of primary cells, as sustained proliferation is generally associated with changes in growth-and survival-related signaling, biosynthetic demand, oxidative state, and energy use (Vander Heiden et al. 2009;Hoxhaj and Manning 2020).”
From Primary cell cultures versus immortalized cell lines: critical comparative insights into biological fidelity and translational applications (2026) · cites this paper as Vander Heiden et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, tumor suppressor pathways such as p53 and LKB1/ AMPK signaling also regulate cellular metabolism (Vander Heiden et al., 2009).”
From Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer (2016) · cites this paper as Vander Heiden et al., 2009
The cited source says what the claim attributes to it.
In the citing paper
“Cancer cells preferentially metabolize glucose by aerobic glycolysis, a phenomenon known as the Warburg effect.”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“Similar to gene expression changes, clustering analysis of proteins with temporal expression dynamics similar to gene expression changes reveals that electron transport chain proteins are downregulated in the first 3 days of reprogramming before a gradual metabolic switch to glycolysis, a characteristic that is typically seen in rapidly proliferating cells 84,97 .”
From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [97]
In the citing paper
“The Warburg effect, a preference for glycolysis and lactate secretion in the presence of oxygen, is an example of a metabolic property under cell-autonomous control by oncogenes in many proliferating cancer cells and tumors (1).”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [1]
In the citing paper
“In 1924, Otto Warburg discovered that cancer cells metabolize glucose differently than cells of normal tissues: that even in conditions of sufficient oxygen availability, cancer cells convert glucose into lactate instead of using glucose for OXPHOS (208).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [208]
In the citing paper
“The carbon economy of a proliferating cell differs dramatically from that of a cell that is quiescent”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Vander Heiden et al., 2009
In the citing paper
“In healthy tissue, the fate of pyruvate is dependent on oxygen availability and mitochondrial respiratory capacity.14”
From The multifaceted contributions of mitochondria to cellular metabolism (2018) · cites this paper as [14]
In the citing paper
“Otto Warburg observed that cancer cells rewire glucose metabolism for lactate synthesis even in normoxia, known as the Warburg Effect.14,21”
From The multifaceted contributions of mitochondria to cellular metabolism (2018) · cites this paper as [14]
In the citing paper
“The recent resurgence of interest in the Warburg hypothesis and cancer energetics (66) emphasizes the dependence of many cancers on glycolysis for energy, creating a high requirement for glucose (or even “glucose addiction”), since ATP generation by glycolysis requires far more glucose than oxidative phosphorylation.”
From Diabetes and Cancer (2010) · cites this paper as [66]
In the citing paper
“This process, also known as the Warburg effect from earlier work in cancer biology, is a common trait of actively proliferating cells (5).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [5]
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An Integrated Genomic Analysis of Human Glioblastoma Multiforme
Parsons, D. W., Jones, S., Zhang, X., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Siu, I.-M., Gallia, G. L., et al. (2008) · Science · doi:10.1126/science.1164382 · Cited by 5,857
IDH1 and IDH2 Mutations in Gliomas
Yan, H., Parsons, D. W., Jin, G., McLendon, R., Rasheed, B. A., Yuan, W., Kos, I., Batinic-Haberle, I., Jones, S., Riggins, G. J., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0808710 · Cited by 5,847
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
(1978) · Biochemical Education · doi:10.1016/0307-4412(78)90049-3 · Cited by 5,073
Why Do Cancers Have High Aerobic Glycolysis?
Gatenby, R. A., & Gillies, R. J. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1478 · Cited by 4,784
The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2007.10.002 · Cited by 4,088
Self-citationOverweight, obesity and cancer: epidemiological evidence and proposed mechanisms
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Metadata
- Authors
- Vander Heiden, M. G., Cantley, L. C., & Thompson, C. B.
- Affiliations
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
- Harvard University (US)
- Abramson Cancer Center (US)
- Corresponding author
- Cantley, Lewis C.
- Thompson, Craig B.
- Venue
- Science
- Published
- 2009-05-22
- Volume
- 324
- Issue
- 5930
- Pages
- 1029-1033
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2849637
- OpenAlex
- W2097259163
- Semantic Scholar
- 5a3b09333eb2968904933e726dc29625e10eb188
- Cited by
- 16,197
- References
- 47
- Citations by year
- 2026: 969 · 2025: 1224 · 2024: 1225 · 2023: 1156 · 2022: 1351 · 2021: 1439 · 2020: 1276 · 2019: 1065 · 2018: 1028 · 2017: 1027 · 2016: 921 · 2015: 823 · 2014: 727 · 2013: 665 · 2012: 535
- FWCI
- 27.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA092660, R01CA105463, T32CA009172)
- National Institute of General Medical Sciences (R01GM056203)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- Warburg effect, aerobic glycolysis, cancer metabolism, cell proliferation, mitochondrial oxidative phosphorylation, ATP production, signaling pathways, cancer-associated mutations, growth regulation
- MeSH terms
- Adenosine Triphosphate, Aerobiosis, Amino Acids, Animals, Glucose, Glycolysis, Humans, Lipids, Mutation, Neoplasms, Nucleotides, Oxidative Phosphorylation, Signal Transduction, Cell Proliferation, Metabolic Networks and Pathways
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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