The DOI matches its Crossref record; 144 of the 145 references it cites were found in a registry or an index; none of the 80 sources its claims cite is checked for support yet.
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Open accessAbstract
Cancer metabolism has long been equated with aerobic glycolysis, seen by early biochemists as primitive and inefficient. Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria, but result from oncogene-directed metabolic reprogramming required to support anabolic growth. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation. No longer can cancer-associated alterations in metabolism be viewed as an indirect response to cell proliferation and survival signals. We contend that altered metabolism has attained the status of a core hallmark of cancer.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that metabolic reprogramming is a core hallmark of cancer, driven by oncogenes and tumor suppressors to support anabolic growth rather than arising passively from mitochondrial damage. It highlights mitochondrial biosynthetic roles, PKM2 and other metabolic enzyme alterations, and oncometabolites such as 2HG that can disrupt epigenetics and differentiation.
Key findings
- Altered metabolism is not merely a secondary response to proliferation signals; it results from active reprogramming by oncogenes and tumor suppressors and is selected during tumorigenesis. Most tumor mitochondria are not defective in oxidative phosphorylation, contrary to Warburg’s original hypothesis.
- PI3K/Akt/mTORC1 and Myc reprogram mitochondrial metabolism for biosynthesis: Akt activates ACL to divert mitochondrial citrate to acetyl-CoA, mTORC1 promotes mitochondrial biogenesis and SREBP-mediated lipogenesis, and Myc enhances glutaminase expression and glutamine addiction. HIF-1 can inhibit PDH via PDK1, blocking glucose carbon entry into mitochondrial citrate and correlating with anti-proliferative effects in some contexts.
- PKM2 is the predominant pyruvate kinase isoform in embryonic tissues and all cancer cells examined to date; it has intrinsically lower enzymatic activity than PKM1 and is sensitive to tyrosine kinase inhibition, proposed to facilitate shunting of glycolytic intermediates into anabolic pathways. At least 11 proteins have been reported to bind PKM2.
- IDH1/IDH2 mutations produce the oncometabolite 2HG, which inhibits α-ketoglutarate-dependent dioxygenases including TET enzymes and histone demethylases, altering DNA and histone methylation and impairing differentiation. IDH2 R140 mutations now account for nearly half of all cases of D-2HG aciduria; succinate and fumarate are also described as oncometabolites.
Methods
- Design: Review article; no primary experimental design is reported.
- Data or sample: Not stated in the paper as a primary dataset; the text synthesizes cited studies across cancer metabolism, oncogene/tumor suppressor signaling, metabolic enzyme isoforms, and oncometabolite biology.
- Main analysis: Conceptual and literature-based synthesis arguing that metabolic reprogramming should be considered a core cancer hallmark.
Limitations
- The paper states that current methods cannot reliably distinguish cytosolic metabolites from mitochondrial and other compartmentalized pools; fractionation methods often cause metabolite leakage, and distinct metabolite pools may exist due to enzyme channeling.
- The paper states that quantitative measurement of metabolic flux remains challenging, including obstacles such as cellular compartmentalization and reliance on complex, incompletely defined cell culture media.
- The paper states that non-cell autonomous effects of tumor metabolism are an emerging challenge, including lactate acidification, possible symbiosis between lactate-producing and lactate-consuming cells, and fatty acid exchange between omental adipocytes and ovarian carcinoma cells. The text also makes evident that unresolved issues remain, such as conflicting conclusions over whether reductive glutamine flux depends primarily on cytosolic IDH1 or mitochondrial IDH2, the role of 2HG in PHD2/HIF regulation, and which alternative NADPH-generating pathways are most important.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
63 Not checked yet · 39 Own interpretation · 13 No basis given
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
“Evidence is also developing for the proposal that proto-oncogenes and tumor suppressors primarily evolved to regulate metabolism.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Introduction
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“We contend that altered metabolism has attained the status of a core hallmark of cancer.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Abstract
plain- Asserted: passes — The authors put it forward as true.
- Checkable: unclear — It is unclear whether it could be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria, but result from oncogene-directed metabolic reprogramming required to support anabolic growth.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Activated PI3K/Akt leads to enhanced glucose uptake and glycolysis (Buzzai et al., 2005; Elstrom et al., 2004).”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > PI3K/Akt/mTORC1 activation: driving anabolic metabolism and tumorigenesis by reprogramming mitochondria
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“In fact, most cancer cells and proliferating normal cells still derive a significant fraction of their ATP through oxidative phosphorylation.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Altered metabolism is a direct response to growth factor signaling
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“Rather than ATP, proliferating cells are in much greater need of reduced carbon and reduced nitrogen, as well as cytosolic NADPH for reductive biosynthetic reactions.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Altered metabolism is a direct response to growth factor signaling
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“However, in contrast to Warburg's original hypothesis, damaged mitochondria are not at the root of the aerobic glycolysis exhibited by most tumor cells.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“In this supply-based model, changes in metabolic fluxes occur in primary response to growth factor signaling, independent of changes in ATP and other mechanisms worked out by early biochemists (Figure 2B).”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Altered metabolism is a direct response to growth factor signaling
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“Most tumor mitochondria are not defective in their ability to carry out oxidative phosphorylation.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
- Probably not a substantial claim. 12
- It may state two separate claims as one. 14
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
“Activation of the PI3K/Akt pathway is perhaps the most common lesion in spontaneous human cancers.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > PI3K/Akt/mTORC1 activation: driving anabolic metabolism and tumorigenesis by reprogramming mitochondria
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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
“It has become clear that anabolic metabolism is under complex regulatory control directed by growth factor signal transduction in non-transformed cells.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Introduction
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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
“Both of these findings are consistent with PKM2 primarily acting as a glycolytic switch that can be rapidly inactivated in tumor cells by multiple mechanisms, all of which facilitate the shunting of glucose carbon/glycolytic intermediates into branching anabolic pathways.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > The primary role of PKM2 expression in proliferating cells is to facilitate anabolic metabolism
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“IDH1 mutations at R132 are not simply loss-of-function for isocitrate and α-ketoglutarate interconversion, but also acquire a novel reductive activity to convert α-ketoglutarate to 2-hydroxyglutarate (2HG)”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Oncogenic mutations in metabolic enzymes: the discovery of IDH1 mutations and the oncometabolite 2-hydroxyglutarate
What the sources say
- Not checked yetcites Dang et al., 2009 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In both cell types, the overexpression of IDH mutants blocked acquisition of mature myeloid markers while increasing the expression of stem cell markers (Figueroa et al., 2010).”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Metabolites as oncogenes: dysregulating epigenetics and cellular differentiation
What the sources say
- Not checked yetcites Figueroa et al., 2010 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Metabolite screening approaches can also distinguish neomorphic IDH mutations from SNPs and sequencing artifacts with no effect on IDH enzyme activity, as well as from an apparently rare subset of loss-of-function, non 2HG-producing IDH mutations”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > 2HG is a biomarker and common feature of both IDH1 and IDH2 mutations
What the sources say
- Not checked yetcites Ward et al., 2011
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Cells expressing oncogenic Myc are glutamine-addicted and undergo apoptosis when glutamine is withdrawn from the culture medium.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Myc activation also impacts mitochondrial metabolism
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a 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
“these data raise the possibility that significant flux through G6PD to generate NADPH is not necessarily critical for cell proliferation or tumorigenesis”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
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
“Historically, the oxidative pentose phosphate pathway, branching off glycolysis at glucose-6-phosphate dehydrogenase (G6PD), has been considered the major NADPH producing pathway.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
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
“It is critical for providing reducing equivalents for fatty acid and cholesterol biosynthesis, as well as for modulating oxidative stress.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably 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
“These findings could all be correct if a mitochondrial-cytosolic NADPH shuttle exists using these enzymes (Figure 6).”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent work has revisited how proliferating cells maintain glycolytic flux by either minimizing ATP production or enhancing ATP consumption.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a 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
“Perhaps elevated succinate and fumarate resulting from SDH and FH mutations can promote tumorigenesis in part through epigenetic modulation.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > 2HG is not the only oncometabolite
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
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
“these findings provide further evidence that IDH mutation can impair differentiation in non-transformed cells from multiple cells of origin, and that this impairment is linked to 2HG-mediated epigenetic dysregulation.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > The oncometabolite 2HG does more than inhibit TET activity and DNA demethylation
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a 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 ability of 2HG to alter epigenetics may reflect its evolutionary ancient status as a signal for elevated glutamine/glutamate metabolism and/or oxygen deficiency.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > 2HG is not the only oncometabolite
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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
“Alternatively, other chromatin-modifying α-ketoglutarate dependent dioxygenase enzymes may be inhibited by 2HG in these cells.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > The oncometabolite 2HG does more than inhibit TET activity and DNA demethylation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“In this alternative pathway, the high-energy phosphate of PEP is not transferred to ADP, but instead to a histidine residue on an upstream glycolytic enzyme. This alternative transfer therefore decouples the PEP→pyruvate conversion from ATP production.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
What the sources say
- Not checked yetcites Vander Heiden et al., 2010
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“glycolysis in proliferating cells is limited by the rate of ATP consumption and not ATP production, as glycolytic enzymes can be inhibited when ATP levels are high (Scholnick et al., 1973)”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Textbook biochemical pathways often do not apply to proliferating cells
What the sources say
- Not checked yetcites Scholnick et al., 1973
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“Even within one subcellular compartment, there may be distinct pools of metabolites resulting from channeling between metabolic enzymes.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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
“many obstacles remain such as cellular compartmentalization and the reliance of most cell culture on complex, incompletely defined media.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“we remain unable to reliably distinguish cytosolic metabolites from those in the mitochondria and other compartments. Current fractionation methods often lead to metabolite leakage.”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“some tumors may exhibit a symbiosis between lactate-producing cells and lactate-consuming cells (Sonveaux et al., 2008)”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
What the sources say
- Not checked yetcites Sonveaux et al., 2008
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“lactate produced by tumor cells can acidify the surrounding microenvironment and potentially promote tumor invasion”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
What the sources say
- Not checked yetcites Sonveaux et al., 2008
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“fatty acid exchange between omental adipocytes and ovarian carcinoma cells has been documented (Nieman et al., 2011)”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
What the sources say
- Not checked yetcites Nieman et al., 2011
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“critical fluxes have been quantified in cultured cancer cells and methods for these analyses continue to improve (DeBerardinis et al., 2007; Mancuso et al., 2004; Yuan et al., 2008)”
§ Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate > Challenges ahead for studying the metabolic hallmark of cancer
What the sources say
- Not checked yetcites DeBerardinis et al., 2007 source
- Not checked yetcites Mancuso et al., 2004
- Not checked yetcites Yuan et al., 2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“The evidence for the necessity of glutamine for cancer progression is conflicted: some studies have reported that tumours can grow well without glutamine [66,67], while others showed that cancers are glutamine-addicted [68,69,70].”
From HIF-1-Independent Mechanisms Regulating Metabolic Adaptation in Hypoxic Cancer Cells (2021) · cites this paper as [68]
In the citing paper
“The previous paradigm of metabolic regulation argued that metabolic pathways were exclusively controlled through allosteric regulation of metabolic enzymes, either by ATP levels or metabolites themselves (the reactive model) (40).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [40]
Citations
Cites
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
Vander Heiden, M. G., Cantley, L. C., & Thompson, C. B. (2009) · Science · doi:10.1126/science.1160809 · Cited by 16,197
Self-citationAn 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
Cancer-associated IDH1 mutations produce 2-hydroxyglutarate
Dang, L., White, D. W., Gross, S., Bennett, B. D., Bittinger, M. A., Driggers, E. M., Fantin, V. R., Jang, H. G., Jin, S., Keenan, M. C., et al. (2009) · Nature · doi:10.1038/nature08617 · Cited by 4,154
Self-citationKim, J.-W., Tchernyshyov, I., Semenza, G. L., & Dang, C. V. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.02.002 · Cited by 3,905
Otto Warburg's contributions to current concepts of cancer metabolism
Koppenol, W. H., Bounds, P. L., & Dang, C. V. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3038 · Cited by 3,427
Xu, W., Yang, H., Liu, Y., Yang, Y., Wang, P., Kim, S.-H., Ito, S., Yang, C., Wang, P., Xiao, M.-T., et al. (2011) · Cancer Cell · doi:10.1016/j.ccr.2010.12.014 · Cited by 2,875
The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth
Christofk, H. R., Vander Heiden, M. G., Harris, M. H., Ramanathan, A., Gerszten, R. E., Wei, R., Fleming, M. D., Schreiber, S. L., & Cantley, L. C. (2008) · Nature · doi:10.1038/nature06734 · Cited by 2,820
Figueroa, M. E., Abdel-Wahab, O., Lu, C., Ward, P. S., Patel, J., Shih, A., Li, Y., Bhagwat, N., Vasanthakumar, A., Fernandez, H. F., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.11.015 · Cited by 2,766
Self-citation
Research works printed but not linked: 11
- Boros, 2000, Cancer Res., 60, 1183
- Choi, 2012, Nat Med.
- Eigenbrodt, 1983, Biomed. Biochim. Acta, 42, S278
- Ferraris, 1988, Am. J. Hum. Genet., 42, 516
- Lu, 2012, Nature
- Mazurek, 2007, Anticancer Res., 27, 3963
- Rempel, 1996, Cancer Res., 56, 2468
- Sonveaux, 2008, J. Clin. Invest., 118, 3930
- Tallal, 1970, Cancer, 25, 306, 10.1002/1097-0142(197002)25:2<306::aid-cncr2820250206>3.0.co;2-h · DOI
- Turcan, 2012, Nature
- Ward, 2011, Oncogene
Cited by
Sorted by citations
Items 101–200 of 1,011
CircACC1 Regulates Assembly and Activation of AMPK Complex under Metabolic Stress
Li, Q., Wang, Y., Wu, S., Zhou, Z., Ding, X., Shi, R., Thorne, R. F., Zhang, X. D., Hu, W., & Wu, M. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.05.009 · Cited by 344
Elucidating cancer metabolic plasticity by coupling gene regulation with metabolic pathways
Jia, D., Lu, M., Jung, K. H., Park, J. H., Yu, L., Onuchic, J. N., Kaipparettu, B. A., & Levine, H. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1816391116 · Cited by 345
Epigenetic modulation of antitumor immunity for improved cancer immunotherapy
Dai, E., Zhu, Z., Wahed, S., Qu, Z., Storkus, W. J., & Guo, Z. S. (2021) · Molecular Cancer · doi:10.1186/s12943-021-01464-x · Cited by 346
Tumor-Suppressor Functions of the TP53 PathwayPreprint
Aubrey, B. J., Strasser, A., & Kelly, G. L. (2016) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a026062 · Cited by 352
Chen, J., & Russo, J. (2012) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2012.06.004 · Cited by 340
Tan, Z., Xie, N., Cui, H., Moellering, D. R., Abraham, E. H., Thannickal, V. J., & Liu, G. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1402469 · Cited by 325
Mitochondria and cancer chemoresistance
Guerra, F., Arbini, A., & Moro, L. (2017) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2017.01.012 · Cited by 331
Cellular metabolic and autophagic pathways: Traffic control by redox signaling
Dodson, M. B., Darley-Usmar, V. M., & Zhang, J. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.05.014 · Cited by 333
Therapeutic targets in cancer cell metabolism and autophagy
Cheong, H., Lü, C., Lindsten, T., & Thompson, C. B. (2012) · Nature Biotechnology · doi:10.1038/nbt.2285 · Cited by 320
Self-citationPark, J. H., Vithayathil, S. A., Kumar, S., Sung, P., Dobrolecki, L. E., Putluri, V., Bhat, V. B., Bhowmik, S. K., Gupta, V. K., Arora, K., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.02.004 · Cited by 316
Tumor microenvironment targeted nanotherapeutics for cancer therapy and diagnosis: A review
Thakkar, S., Sharma, D., Kalia, K., & Tekade, R. K. (2019) · Acta Biomaterialia · doi:10.1016/j.actbio.2019.09.009 · Cited by 321
Glutamine-based PET imaging facilitates enhanced metabolic evaluation of gliomas in vivo
Venneti, S., Dunphy, M. P., Zhang, H., Pitter, K. L., Zanzonico, P., Campos, C., Carlin, S., Rocca, G. L., Lyashchenko, S. K., Plöessl, K., et al. (2015) · Science Translational Medicine · doi:10.1126/scitranslmed.aaa1009 · Cited by 326
Self-citationGut bacteria signaling to mitochondria in intestinal inflammation and cancer
Jackson, D. N., & Theiss, A. L. (2020) · Gut Microbes · doi:10.1080/19490976.2019.1592421 · Cited by 312
Tan, Y., Li, J., Zhao, G., Huang, K., Cárdenas, H., Wang, Y., Matei, D. E., & Cheng, J. (2022) · Nature Communications · doi:10.1038/s41467-022-32101-w · Cited by 322
Dysregulated metabolism contributes to oncogenesis
Hirschey, M. D., DeBerardinis, R. J., Diehl, A. M., Drew, J. E., Frezza, C., Green, M. F., Jones, L. W., Ko, Y. H., Le, A., Lea, M. A., et al. (2015) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2015.10.002 · Cited by 316
Koppula, P., Zhang, Y., Shi, J., Li, W., & Gan, B. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.798405 · Cited by 302
A long noncoding RNA connects c-Myc to tumor metabolism
Hung, C.-L., Wang, L., Yu, Y., Chen, H.-W., Srivastava, S. K., Petrovics, G., & Kung, H.-J. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1415669112 · Cited by 303
Ventura, R., Mordec, K., Waszczuk, J., Wang, Z., Lai, J., Fridlib, M., Buckley, D., Kemble, G., & Heuer, T. S. (2015) · EBioMedicine · doi:10.1016/j.ebiom.2015.06.020 · Cited by 301
Tumor suppressor p53 and metabolism
Liu, J., Zhang, C., Hu, W., & Feng, Z. (2018) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mjy070 · Cited by 313
Abrogating cholesterol esterification suppresses growth and metastasis of pancreatic cancer
Li, J., Gu, D., Lee, S. S.-Y., Song, B., Bandyopadhyay, S., Chen, S., Konieczny, S. F., Ratliff, T. L., Liu, X., Xie, J., et al. (2016) · Oncogene · doi:10.1038/onc.2016.168 · Cited by 300
Regulators of mitochondrial dynamics in cancer
Senft, D., & Ronai, Z. A. (2016) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2016.02.001 · Cited by 306
Masson, N., & Ratcliffe, P. J. (2014) · Cancer & Metabolism · doi:10.1186/2049-3002-2-3 · Cited by 305
Willems, L., Jacque, N., Jacquel, A., Neveux, N., Maciel, T. T., Lambert, M., Schmitt, A., Poulain, L., Green, A. S., Uzunov, M., et al. (2013) · Blood · doi:10.1182/blood-2013-03-493163 · Cited by 295
Metabolism shapes the tumor microenvironment
Reina‐Campos, M., Moscat, J., & Díaz-Meco, M. T. (2017) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2017.05.006 · Cited by 292
Pastò, A., Bellio, C., Pilotto, G., Ciminale, V., Silic‐Benussi, M., Guzzo, G., Rasola, A., Frasson, C., Nardo, G., Zulato, E., et al. (2014) · Oncotarget · doi:10.18632/oncotarget.2010 · Cited by 298
The fat side of prostate cancer
Zadra, G., Photopoulos, C., & Loda, M. F. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2013.03.010 · Cited by 301
Agnihotri, S., & Zadeh, G. M. (2015) · Neuro-Oncology · doi:10.1093/neuonc/nov125 · Cited by 302
ROS homeostasis and metabolism: a critical liaison for cancer therapy
Kim, J., Kim, J., & Bae, J. (2016) · Experimental & Molecular Medicine · doi:10.1038/emm.2016.119 · Cited by 304
den Boon, J. A., Pyeon, D., WANG, S. S., Horswill, M. A., SCHIFFMAN, M. H., Sherman, M. E., Zuna, R. E., Wang, Z., Hewitt, S. M., Pearson, R., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1509322112 · Cited by 293
ERGO: A pilot study of ketogenic diet in recurrent glioblastoma
Rieger, J., Bähr, O., Maurer, G. D., Hattingen, E., Franz, K., Brucker, D. P., Walenta, S., Kämmerer, U., Coy, J. F., Weller, M., et al. (2014) · International Journal of Oncology · doi:10.3892/ijo.2014.2382 · Cited by 284
Citrate – new functions for an old metabolite
Iacobazzi, V., & Infantino, V. (2014) · Biological Chemistry · doi:10.1515/hsz-2013-0271 · Cited by 295
Circulating tumor cell isolation for cancer diagnosis and prognosis
Deng, Z., Wu, S., Wang, Y., & Shi, D. (2022) · EBioMedicine · doi:10.1016/j.ebiom.2022.104237 · Cited by 291
SirT3 Regulates the Mitochondrial Unfolded Protein Response
Papa, L., & Germain, D. (2013) · Molecular and Cellular Biology · doi:10.1128/mcb.01337-13 · Cited by 292
Neutrophil Extracellular Traps Drive Mitochondrial Homeostasis in Tumors to Augment Growth
Yazdani, H. O., Roy, E., Comerci, A. J., van der Windt, D. J., Zhang, H., Huang, H., Loughran, P., Shiva, S., Geller, D. A., Bartlett, D. L., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-19-0800 · Cited by 280
Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management
Jin, P., Jiang, J., Zhou, L., Huang, Z., Nice, E. C., Huang, C., & Fu, L. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01313-4 · Cited by 299
Jia, D., Park, J. E., Jung, K., Levine, H., & Kaipparettu, B. A. (2018) · Cells · doi:10.3390/cells7030021 · Cited by 283
Tan, Z., Xiao, L., Tang, M., Bai, F., Li, J., Li, L., Shi, F., Li, N., Li, Y., Du, Q., et al. (2018) · Theranostics · doi:10.7150/thno.21451 · Cited by 279
The Metabolic Basis of Pulmonary Arterial Hypertension
Sutendra, G., & Michelakis, E. D. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.01.004 · Cited by 271
Lim, S., Li, C., Xia, W., Lee, H., Chang, S.-S., Shen, J., Hsu, J. L., Raftery, D., Djukovic, D., Gu, H., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-2478 · Cited by 270
Arginine dependence of tumor cells: targeting a chink in cancer’s armor
Patil, M. D., Bhaumik, J., Babykutty, S., Banerjee, U. C., & Fukumura, D. (2016) · Oncogene · doi:10.1038/onc.2016.37 · Cited by 272
Wu, H., Liu, B., Chen, Z., Li, G., & Zhang, Z. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-2426-z · Cited by 267
The good and the bad faces of STAT1 in solid tumours
Meissl, K., Macho‐Maschler, S., Müller, M. M., & Strobl, B. (2015) · Cytokine · doi:10.1016/j.cyto.2015.11.011 · Cited by 272
Cyclin B1/CDK1-regulated mitochondrial bioenergetics in cell cycle progression and tumor resistance
Xie, B., Wang, S., Jiang, N., & Li, J. J. (2018) · Cancer Letters · doi:10.1016/j.canlet.2018.11.019 · Cited by 268
Microenvironment and tumor cell plasticity: An easy way out
Taddei, M. L., Giannoni, E., Comito, G., & Chiarugi, P. (2013) · Cancer Letters · doi:10.1016/j.canlet.2013.01.042 · Cited by 272
The complexity of p53-mediated metabolic regulation in tumor suppression
Liu, Y., & Gu, W. J. (2021) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2021.03.010 · Cited by 267
Hart, P. C., Mao, M., de Abreu, A. L. P., Ansenberger-Fricano, K., Ekoue, D. N., Ganini, D., Kajdacsy-Balla, A., Diamond, A. M., Minshall, R. D., Consolaro, M. E. L., et al. (2015) · Nature Communications · doi:10.1038/ncomms7053 · Cited by 260
Cunningham, J. T., Moreno, M. V., Lodi, A., Ronen, S. M., & Ruggero, D. (2014) · Cell · doi:10.1016/j.cell.2014.03.052 · Cited by 260
Cellular and metabolic functions for autophagy in cancer cells
Kenific, C. M., & Debnath, J. (2014) · Trends in Cell Biology · doi:10.1016/j.tcb.2014.09.001 · Cited by 270
Pyruvate Kinase Isoform Expression Alters Nucleotide Synthesis to Impact Cell Proliferation
Lunt, S. Y., Muralidhar, V., Hosios, A. M., Israelsen, W. J., Gui, D. Y., Newhouse, L., Ogrodzinski, M. P., Hecht, V. C., Xu, K., Acevedo, P. N. M., et al. (2014) · Molecular Cell · doi:10.1016/j.molcel.2014.10.027 · Cited by 263
Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) as a therapeutic strategy in cancer
Sampath, D., Zabka, T. S., Misner, D. L., O’Brien, T., & Dragovich, P. S. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.02.004 · Cited by 258
Metabolic reprogramming and therapeutic resistance in primary and metastatic breast cancer
Liu, S., Zhang, X., Wang, W., Li, X., Sun, X., Zhao, Y., Wang, Q., Li, Y., Hu, F., & Ren, H. (2024) · Molecular Cancer · doi:10.1186/s12943-024-02165-x · Cited by 300
Penny, H. L., Sieow, J. L., Adriani, G., Yeap, W. H., See, P., Luis, B. S., Lee, B. T. K., Lee, T. K., Mak, S. Y., Ho, Y. S., et al. (2016) · OncoImmunology · doi:10.1080/2162402x.2016.1191731 · Cited by 261
Hou, P.-P., Luo, L.-J., Chen, H., Chen, Q.-T., Bian, X., Wu, S.-F., Zhou, J.-X., Zhao, W., Liu, J., Wang, X., et al. (2020) · Molecular Cell · doi:10.1016/j.molcel.2020.05.004 · Cited by 256
A graph neural network model to estimate cell-wise metabolic flux using single-cell RNA-seq dataPreprint
Alghamdi, N., Chang, W., Dang, P., Lu, X., Wan, C., Gampala, S., Huang, Z., Wang, J., Ma, Q., Zang, Y., et al. (2021) · Genome Research · doi:10.1101/gr.271205.120 · Cited by 271
Li, L., & Li, W. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.01.004 · Cited by 257
Peck, B., Schug, Z. T., Zhang, Q., Dankworth, B., Jones, D. T., Smethurst, E. A., Patel, R., Mason, S. M., Jiang, M., Saunders, R. E., et al. (2016) · Cancer & Metabolism · doi:10.1186/s40170-016-0146-8 · Cited by 248
Drug resistance in pancreatic cancer: Impact of altered energy metabolism
Grasso, C., Jansen, G., & Giovannetti, E. (2017) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2017.03.026 · Cited by 260
Metabolic regulation of macrophage phenotype and function
Saha, S., Shalova, I. N., & Biswas, S. K. (2017) · Immunological Reviews · doi:10.1111/imr.12603 · Cited by 260
Metabolic enzyme PFKFB4 activates transcriptional coactivator SRC-3 to drive breast cancer
Dasgupta, S., Rajapakshe, K., Zhu, B., Nikolai, B. C., Yi, P., Putluri, N., Choi, J. M., Jung, S. Y., Coarfa, C., Westbrook, T. F., et al. (2018) · Nature · doi:10.1038/s41586-018-0018-1 · Cited by 252
Pierotti, M. A., Berrino, F., Gariboldi, M., Melani, C. C., Mogavero, A., Negri, T., Pasanisi, P., & Pilotti, S. (2012) · Oncogene · doi:10.1038/onc.2012.181 · Cited by 253
Cunniff, B., McKenzie, A. J., Heintz, N. H., & Howe, A. K. (2016) · Molecular Biology of the Cell · doi:10.1091/mbc.e16-05-0286 · Cited by 252
Lauvrak, S. U., Munthe, E., Kresse, S. H., Stratford, E. W., Namløs, H. M., Meza‐Zepeda, L. A., & Myklebost, O. (2013) · British Journal of Cancer · doi:10.1038/bjc.2013.549 · Cited by 252
MicroRNA-26a regulates insulin sensitivity and metabolism of glucose and lipids
Fu, X., Dong, B., Tian, Y., Lefèbvre, P., Meng, Z., Wang, X., Pattou, F. N., Han, W., Wang, X., Lou, F., et al. (2015) · Journal of Clinical Investigation · doi:10.1172/jci75438 · Cited by 253
Classification of mitocans, anti-cancer drugs acting on mitochondria
Neužil, J., Dong, L., Rohlena, J., Truksa, J., & Ralph, S. J. (2012) · Mitochondrion · doi:10.1016/j.mito.2012.07.112 · Cited by 255
Kalyanaraman, B. (2017) · Redox Biology · doi:10.1016/j.redox.2017.04.018 · Cited by 254
Lucarelli, G. T., Loizzo, D., Franzin, R., Battaglia, S., Ferro, M., Cantiello, F., Castellano, G., Bettocchi, C., Ditonno, P., & Battaglia, M. (2019) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2019.1607729 · Cited by 249
The Warburg effect: Insights from the past decade
Upadhyay, M., Samal, J., Kandpal, M., Singh, O. V., & Vivekanandan, P. (2012) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2012.11.003 · Cited by 252
Cancer metabolism: Key players in metabolic reprogramming
Soga, T. (2012) · Cancer Science · doi:10.1111/cas.12085 · Cited by 247
Targeting cancer stem cells to suppress acquired chemotherapy resistance
Vidal, S. J., Rodríguez-Bravo, V., Galsky, M. D., Cordon‐Cardo, C., & Domenech, J. M. D. (2013) · Oncogene · doi:10.1038/onc.2013.411 · Cited by 244
Zhou, G., Wang, J., Zhao, M., Xie, T., Tanaka, N., Sano, D., Patel, A. A., Ward, A. M., Sandulache, V. C., Jasser, S. A., et al. (2014) · Molecular Cell · doi:10.1016/j.molcel.2014.04.024 · Cited by 248
Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment
Tanaka, K., Sasayama, T., Irino, Y., Takata, K., Nagashima, H., Satoh, N., Kyotani, K., Mizowaki, T., Imahori, T., Ejima, Y., et al. (2015) · Journal of Clinical Investigation · doi:10.1172/jci78239 · Cited by 249
Metabolic reprogramming in triple-negative breast cancer
Wang, Z., Jiang, Q., & Dong, C. (2020) · Cancer Biology and Medicine · doi:10.20892/j.issn.2095-3941.2019.0210 · Cited by 248
“This rewired metabolic network depends on the dysregulation of many key enzymes, such as pyruvate kinase muscle isozyme M2 (PKM2), which redirects glycolytic intermediates into the anabolic pathway 7 .”
BackgroundLucarelli, G. T., Galleggiante, V., Rutigliano, M., Sanguedolce, F., Cagiano, S., Bufo, P., Lastilla, G., Maiorano, E., Ribatti, D., Giglio, A., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.3823 · Cited by 243
Heterogeneity in Cancer Metabolism: New Concepts in an Old Field
Gentric, G., Mieulet, V., & Mechta‐Grigoriou, F. (2016) · Antioxidants and Redox Signaling · doi:10.1089/ars.2016.6750 · Cited by 248
Metabolism in physiological cell proliferation and differentiation
Agathocleous, M., & Harris, W. A. (2013) · Trends in Cell Biology · doi:10.1016/j.tcb.2013.05.004 · Cited by 245
Pyruvate Kinase M2: Multiple Faces for Conferring Benefits on Cancer Cells
Tamada, M., Suematsu, M., & Saya, H. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-12-0859 · Cited by 238
Yoshida, G. J. (2017) · Journal of Hematology & Oncology · doi:10.1186/s13045-017-0436-9 · Cited by 239
Amino acid metabolism in hematologic malignancies and the era of targeted therapy
Tabe, Y., Lorenzi, P. L., & Konopleva, M. Y. (2019) · Blood · doi:10.1182/blood.2019001034 · Cited by 244
The Potential Health Benefits of the Ketogenic Diet: A Narrative Review
Dowis, K., & Banga, S. (2021) · Nutrients · doi:10.3390/nu13051654 · Cited by 253
Kalyanaraman, B., Cheng, G., Hardy, M., Ouari, O., López, M., Joseph, J., Zielonka, J., & Dwinell, M. B. (2017) · Redox Biology · doi:10.1016/j.redox.2017.09.020 · Cited by 239
MYC inhibition induces metabolic changes leading to accumulation of lipid droplets in tumor cells
Zirath, H., Frenzel, A., Oliynyk, G., Segerström, L., Westermark, U., Larsson, K., Persson, M. M., Hultenby, K. R., Lehtiö, J., Einvik, C., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1222404110 · Cited by 229
Lactate promotes glutamine uptake and metabolism in oxidative cancer cells
Pérez-Escuredo, J., Dadhich, R. K., Dhup, S., Cacace, A., Van Hée, V. F., De Saedeleer, C. J., Sboarina, M., Rodriguez, F., Fontenille, M.-J., Brisson, L., et al. (2016) · Cell Cycle · doi:10.1080/15384101.2015.1120930 · Cited by 231
Nuclear GTPSCS functions as a lactyl-CoA synthetase to promote histone lactylation and gliomagenesis
Liu, R., Ren, X., Park, Y. E., Feng, H., Sheng, X., Song, X., AminiTabrizi, R., Shah, H., Li, L., Zhang, Y., et al. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2024.11.005 · Cited by 253
Cancer Metabolism: Current Understanding and Therapies
Counihan, J. L., Grossman, E. A., & Nomura, D. K. (2018) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00775 · Cited by 236
MYC-Driven Pathways in Breast Cancer Subtypes
Fallah, Y., Brundage, J., Allegakoen, P., & Shajahan‐Haq, A. N. (2017) · Biomolecules · doi:10.3390/biom7030053 · Cited by 226
B7-H3 promotes aerobic glycolysis and chemoresistance in colorectal cancer cells by regulating HK2
Shi, T., Ma, Y., Cao, L., Zhan, S., Xu, Y., Fu, F., Liu, C., Zhang, G., Wang, Z., Wang, R., et al. (2019) · Cell Death and Disease · doi:10.1038/s41419-019-1549-6 · Cited by 228
The Potential of Metabolomics in Biomedical Applications
González-Covarrubias, V., Martínez‐Martínez, E., & del Bosque‐Plata, L. (2022) · Metabolites · doi:10.3390/metabo12020194 · Cited by 249
Yang, H., Zhou, L., Shi, Q., Zhao, Y., Lin, H., Zhang, M., Zhao, S., Yang, Y. A., Ling, Z., Guan, K., et al. (2015) · The EMBO Journal · doi:10.15252/embj.201591041 · Cited by 225
Metabolic Dependencies in RAS -Driven Cancers
Kimmelman, A. C. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2425 · Cited by 230
Eisenreich, W., Rudel, T., Heesemann, J., & Goebel, W. (2019) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2019.00042 · Cited by 229
Metabolic Reprogramming of Cancer Cells during Tumor Progression and Metastasis
Ohshima, K., & Morii, E. (2021) · Metabolites · doi:10.3390/metabo11010028 · Cited by 236
Linehan, W. M., & Rouault, T. A. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-13-0304 · Cited by 226
Embryonic stem cell and induced pluripotent stem cell: an epigenetic perspective
Liang, G., & Zhang, Y. (2012) · Cell Research · doi:10.1038/cr.2012.175 · Cited by 232
No Parkin Zone: Mitophagy without Parkin
Villa, E., Marchetti, S., & Ricci, J. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.07.004 · Cited by 229
Dihydropyrimidine Accumulation Is Required for the Epithelial-Mesenchymal Transition
Shaul, Y. D., Freinkman, E., Comb, W. C., Cantor, J. R., Tam, W. L., Thiru, P., Kim, D., Kanarek, N., Pacold, M. E., Chen, W. W., et al. (2014) · Cell · doi:10.1016/j.cell.2014.07.032 · Cited by 223
Burns, J. S., & Manda, G. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18122755 · Cited by 230
Wen, Y., Xiong, X., Zaytseva, Y. Y., Napier, D. L., Vallee, E., Li, A. T., Wang, C., Weiss, H. L., Evers, B. M., & Gao, T. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-0330-6 · Cited by 225
Fujiwara, N., Nakagawa, H., Enooku, K., Kudo, Y., Hayata, Y., Nakatsuka, T., Tanaka, Y., Tateishi, R., Hikiba, Y., Misumi, K., et al. (2018) · Gut · doi:10.1136/gutjnl-2017-315193 · Cited by 226
ACSL4 reprograms fatty acid metabolism in hepatocellular carcinoma via c-Myc/SREBP1 pathway
Chen, J., Ding, C., Chen, Y., Hu, W., Yu, C., Peng, C., Feng, X., Cheng, Q., Wu, W., Lu, Y., et al. (2020) · Cancer Letters · doi:10.1016/j.canlet.2020.12.019 · Cited by 222
Oncometabolites in renal cancer
Yong, C., Stewart, G. D., & Frezza, C. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0210-z · Cited by 216
Metadata
- Authors
- Ward, P. S., & Thompson, C. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Thompson, Craig B.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 21
- Issue
- 3
- Pages
- 297-308
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3311998
- OpenAlex
- W2052543023
- Semantic Scholar
- 9802ecaa29613434cd7f6f7fa0e72b84a26c9d29
- Cited by
- 3,233
- References
- 145
- Citations by year
- 2026: 149 · 2025: 170 · 2024: 216 · 2023: 204 · 2022: 269 · 2021: 271 · 2020: 295 · 2019: 244 · 2018: 256 · 2017: 235 · 2016: 213 · 2015: 248 · 2014: 228 · 2013: 169 · 2012: 63
- FWCI
- 17.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 994 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Pennsylvania
- National Institutes of Health
- National Cancer Institute
- 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 › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- cancer metabolism, metabolic reprogramming, aerobic glycolysis, Warburg effect, anabolic metabolism, signal transduction, cell differentiation, cancer hallmarks, mitochondrial damage
- MeSH terms
- Cell Differentiation, Humans, Isoenzymes, Mitochondria, Models, Biological, Neoplasms, Biomarkers, Tumor, Signal Transduction, Proto-Oncogene Proteins c-myc, Alternative Splicing, Evolution, Molecular, Epigenesis, Genetic, Cell Proliferation
About these checks
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.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
