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.
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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.
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Claims the paper makes
63 Not checked yet · 39 Own interpretation · 13 No basis given
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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
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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
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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
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“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
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“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
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“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
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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
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“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
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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
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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.
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- Probably not a substantial claim. 12
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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.
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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
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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
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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
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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.
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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
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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
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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
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“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
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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.
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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
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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
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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
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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
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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.
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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.
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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
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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.
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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
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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.
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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.
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“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.
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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
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“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.
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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.
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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.
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Claims other papers make about this one
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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
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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
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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.
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