The DOI matches its Crossref record; 241 of the 254 references it cites were found in a registry or an index, and 1 are not checked yet; none of the 254 sources its claims cite is checked for support yet.
The Emerging Hallmarks of Cancer Metabolism
Open accessAbstract
Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and indirect consequence of oncogenic mutations. A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass. The alterations in intracellular and extracellular metabolites that can accompany cancer-associated metabolic reprogramming have profound effects on gene expression, cellular differentiation and the tumor microenvironment. In this Review, we have organized known cancer-associated metabolic changes into six hallmarks: (1) deregulated uptake of glucose and amino acids, (2) use of opportunistic modes of nutrient acquisition, (3) use of glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, (4) increased demand for nitrogen, (5) alterations in metabolite-driven gene regulation, and (6) metabolic interactions with the microenvironment. While few tumors display all six hallmarks, most display several. The specific hallmarks exhibited by an individual tumor may ultimately contribute to better tumor classification and aid in directing treatment.
Checked 2026-10-09 · 1 reference not checked yet
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Written from the paper’s full text.
TL;DR
This review organizes known cancer-associated metabolic changes into six hallmarks: deregulated uptake of glucose and amino acids, opportunistic modes of nutrient acquisition, use of glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, increased demand for nitrogen, alterations in metabolite-driven gene regulation, and metabolic interactions with the microenvironment. The authors argue that while few tumors display all six hallmarks, most display several, and the specific hallmarks exhibited may aid tumor classification and treatment direction.
Key findings
- Cancer cells acquire nutrients through oncogene-driven constitutive uptake: PI3K/Akt signaling promotes GLUT1 expression and translocation and potentiates hexokinase and phosphofructokinase, while c-myc drives glutamine transporter (ASCT2, SN2) and glutaminase (GLS1) expression; Rb loss upregulates ASCT2 and GLS1 via E2F.
- Opportunistic nutrient acquisition allows survival under scarcity: Ras- or c-Src-driven macropinocytosis enables lysosomal degradation of extracellular protein (albumin at 20–30 mg/mL supports KRASG12D MEF proliferation without leucine), and mTORC1 inhibitors enhance this route — rapamycin suppresses proliferation at the tumor margin but enhances it in the poorly vascularized tumor core.
- Proliferating cells divert glycolytic intermediates into biosynthesis: cancer cells may use as much as 50% of glucose-derived carbon for serine biosynthesis, and stepwise oxidation of one-carbon-THF species can produce up to 50% of cellular NADPH; PKM2 (rather than PKM1) predominates in essentially all cancer cells and is inhibited by tyrosine phosphorylation and activated by serine.
- Metabolite-driven gene regulation links metabolism to epigenetics: mutant IDH1/IDH2 produce 2-HG that competitively inhibits α-ketoglutarate-dependent dioxygenases, and SDH/FH loss accumulates succinate/fumarate, all producing hypermethylation phenotypes; lactate accumulation promotes M2 macrophage polarization, angiogenesis, and immune-permissive microenvironments.
Methods
- Narrative review/Perspective synthesizing published literature on cancer metabolism; the authors state they organize known cancer-associated metabolic changes into six hallmarks.
- No primary data, sample, or statistical analysis is reported; evidence is drawn from cited studies across cell lines, mouse models, patient samples, and clinical imaging (e.g., 18F-FDG and 18F-glutamine PET).
- Not stated in the paper for any systematic search strategy, inclusion criteria, or quantitative synthesis.
Limitations
- The paper states that most studies to date have focused on glucose and glutamine metabolism, and that the contributions of other nutrients (sulfur-containing amino acids, essential fatty acids, choline, trace metals, vitamins, and microbiota-derived metabolites) are only beginning to be understood.
- The paper notes that cell lineage context and potential secondary effects of adaptation to tissue culture conditions may influence findings such as the choice of anaplerotic substrate (glutamine vs. glucose-derived pyruvate carboxylation).
- Evident from the text: as a narrative review without primary data or systematic methodology, the six-hallmark framework is an organizing proposal rather than an empirically validated classification, and the authors state that few tumors display all six hallmarks.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
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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
“Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and indirect consequence of oncogenic mutations.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIn the paper
“In such a manner, intracellular glutamine may facilitate the import of a broad range of LAT1 substrates, including leucine, isoleucine, valine, methionine, tyrosine, tryptophan and phenylalanine”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Yanagida et al., 2001 source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“when deprived of growth factors, hematopoietic and neuronal cells fail to consume glucose in quantities sufficient to even maintain cellular bioenergetics”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“the optimal growth of cultured HeLa cells requires a 10- to a 100-fold molar excess of glutamine in culture medium relative to other amino acids”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Eagle, 1955 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe 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
“Thus, glutamine provides the nitrogen required for the biosynthesis of purine and pyrimidine nucleotides, glucosamine-6-phosphate, as well as non-essential amino acids.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“glutamine was found to be the most rapidly consumed amino acid by Ehrlich ascites carcinomas as well as by a number of hepatomas and carcinosarcomas proliferating in vivo”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Marquez et al., 1989 source
- Not checked yetcites Sauer et al., 1982
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe 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
“Glutamine, a second principal growth-supporting substrate contributes not only carbon, but also reduced nitrogen for the de novo biosynthesis of a number of diverse nitrogen-containing compounds.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“numerous tumorigenic contexts are associated with the depletion of glutamine from the tumor environment as compared to the corresponding normal tissue”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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 alterations in intracellular and extracellular metabolites that can accompany cancer-associated metabolic reprogramming have profound effects on gene expression, cellular differentiation and the tumor microenvironment.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearThe 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
“Through the catabolism of glucose and glutamine, a cell maintains pools of diverse carbon intermediates, which are utilized as building blocks for the assembly of various macromolecules.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 87
- Probably not a substantial claim. 15
In the paper
“This observation has been confirmed in a variety of tumor contexts and shown to correlate with poor tumor prognosis”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Som et al., 1980
Strength:plain· not yet calibratedCausal:correlational· 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
“tumorigenesis-associated metabolic alterations encompass all stages of cell-metabolite interaction, (a) affecting the metabolite influx through conferring an increased ability to acquire the necessary nutrients; (b) shaping the way the nutrients are preferentially assigned to metabolic pathways that contribute to cellular tumorigenic properties, as well as (c) exerting long-ranging effects on”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INTRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Normally, despite being surrounded by nutrient-rich plasma and the extracellular fluid, metazoan cells do not import nutrients in a constitutive manner. On the contrary, nutrient uptake is strictly regulated by growth factor signaling”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Thompson, 2011 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“controlled oxidation of carbon skeletons of glucose and glutamine allows a cell to capture their reducing power either in the form of NADH and FADH2, which mediate the transfer of electrons to the electron transport chain to fuel ATP generation, or in the form of a related cofactor NADPH, which provides reducing power for a wide variety of biosynthetic reactions, as well as helps maintain cellular”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Positron emission tomography (PET)-based imaging of the uptake of a radioactive fluorine-labeled glucose analog, 18F-fluorodeoxyglucose (18F-FDG) has been successfully used in the clinic for tumor diagnosis and staging, as well as for monitoring responsiveness to treatment”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Almuhaideb et al., 2011
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“This, in turn, negatively affects cell size, mitochondrial potential and ATP generation – all despite the abundance of glucose in the culture medium”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Rathmell et al., 2000
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“In order to fulfill the biosynthetic demands associated with proliferation, a cell must increase the import of nutrients from the environment.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
“Two principal nutrients that support survival and biosynthesis in mammalian cells are glucose and glutamine.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“mTORC1 inhibitors greatly increase the cellular ability to recover amino acids from captured extracellular protein and enhance their growth in the absence of essential amino acids”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
What the sources say
- Not checked yetcites Palm et al., 2015
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“free amino acids can be recovered from the engulfment and digestion of entire living cells via a process known as entosis (Figure 3B), as well as from phagocytosis of apoptotic cellular corpses”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
What the sources say
- Not checked yetcites Krajcovic et al., 2013 source
- Not checked yetcites Stolzing and Grune, 2004
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“c-myc induces the transcription of glutamine transporters ASCT2 and SN2, and in addition, promotes expression of glutamine-utilizing enzymes glutaminase (GLS1), phosphoribosyl pyrophosphate synthetase (PRPS2) and carbamoyl-phosphate synthetase 2 (CAD)”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Eberhardy and Farnham, 2001
- Not checked yetcites Gao et al., 2009 source
- Not checked yetcites Mannava et al., 2008
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“While rapamycin suppresses cancer cell proliferation at the tumor margin where the vascular delivery of nutrients is effective, rapamycin enhances cell proliferation within the poorly-vascularized tumor core by promoting enhanced lysosomal degradation of extracellular proteins”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
What the sources say
- Not checked yetcites Palm et al., 2015
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“subsequent investigations into the mitochondrial status of tumor cells have shown that by and large, tumor cells possess functional mitochondria and retain the ability to conduct oxidative phosphorylation.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Thus, KRAS-mutant cells may not only have a nutritional advantage over their non-mutant neighbors, but also actively eliminate the latter.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“exogenous expression of a constitutively active form of Akt alone can stimulate glycolysis and is sufficient to restore cell size, viability, mitochondrial potential and ATP levels in growth factor-deprived cells in a manner that is dependent upon the presence of glucose in the culture medium”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Plas et al., 2001
- Not checked yetcites Rathmell et al., 2003 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“These observations suggest that, rather than being an adaptation to a defect in respiration, the Warburg effect is a regulated metabolic state and may, in fact, be beneficial during a time of increased biosynthetic demand.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Culturing mammary epithelial cells under conditions where the cells are detached from the extracellular matrix compromises glucose uptake and results in a depressed mitochondrial potential and decreased ATP levels”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Grassian et al., 2011
- Not checked yetcites Schafer et al., 2009 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Akt potentiates the activity of the hexokinase (HK), which phosphorylates glucose molecules, thus preventing their efflux back into the extracellular space, as well as of the phosphofructokinase (PFK) enzyme, which catalyzes the key irreversible step of glycolysis”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Deprez et al., 1997
- Not checked yetcites Gottlob et al., 2001
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Other oncogenic signaling proteins - notably, Ras, have been found to upregulate GLUT1 mRNA expression and increase cellular glucose consumption”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Murakami et al., 1992
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
“Thus, the utilization of extracellular protein as nutrients is repressed by mTORC1 under amino acid-replete conditions and is only utilized as an emergency source in conditions when free amino acids are insufficient.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“generation of palmitic acid consumes 14 reducing equivalents, while building a cholesterol molecule requires 26”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Lunt and Vander Heiden, 2011 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the 18F-FDG-PET signal intensity in tumors correlates closely with the level of PI3K/Akt pathway activity, and is attenuated by PI-3 kinase and receptor tyrosine kinase inhibitors”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Benz et al., 2011
- Not checked yetcites Lheureux et al., 2013
- Not checked yetcites Ma et al., 2009
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“In contrast to the effect of KRASG12D, PI3K/Akt signaling does not promote cellular utilization of extracellular protein, despite the ability of this pathway to stimulate the uptake of low molecular weight nutrients”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF OPPORTUNISTIC MODES OF NUTRIENT ACQUISITION
What the sources say
- Not checked yetcites Palm et al., 2015
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PI3K/Akt signaling promotes both the expression of glucose transporter GLUT1 mRNA and the translocation of GLUT1 protein from the endomembranes to the cell surface”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > DEREGULATED UPTAKE OF GLUCOSE AND AMINO ACIDS
What the sources say
- Not checked yetcites Barthel et al., 1999
- Not checked yetcites Wieman et al., 2007
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“A designated donor of reducing equivalents that is used in cellular biosynthetic reactions is NADPH.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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 first committed step of hexosamine biosynthesis is a glutamine fructose-6-phospate aminotransferase 1 (GFPT1)-catalyzed production of glucosamine-6-phosphate from fructose-6-phosphate and glutamine.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“A rate-limiting serine biosynthesis enzyme, 3-phosphoglycerate dehydrogenase (PHGDH), is frequently focally amplified in breast cancer and melanoma and is required for the growth of PHGDH-amplified cells in vitro as well as in vivo”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast to the proliferating bulk of a tumor, accumulating evidence suggests that quiescent subpopulations of tumor cells are markedly less glycolytic and exhibit higher dependence on oxidative phosphorylation, as well as elevated expression of mitochondrial respiratory components.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites LeBleu et al., 2014
- Not checked yetcites Viale et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“glycolytic intermediates leave glycolysis to take part in diverse biosynthetic reactions; accordingly, the rate-limiting enzymes within branching pathways of glycolysis are frequently upregulated in tumors.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While the de novo biosynthesis of fatty acids is low in normal adult tissues – with the exception of lipogenic tissues such as liver, adipose tissue or mammary epithelium in the period of lactation, tumorigenesis is associated with a dramatic increase in lipid production (Li and Cheng, 2014; Menendez and Lupu, 2007).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Li and Cheng, 2014
- Not checked yetcites Menendez and Lupu, 2007
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“By using FAD as an electron acceptor, the mGPDH-catalyzed reaction reduces net mitochondrial electrical chemical potential from NADH generated via glycolysis.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, increased ROS levels facilitate the activation of HIF1α and NRF2 transcription factors, thus promoting transcriptional programs that further contribute to tumorigenesis (Bertout et al., 2008; Sporn and Liby, 2012).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Bertout et al., 2008
- Not checked yetcites Sporn and Liby, 2012 source
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
“First in the series of these branching pathways is the pentose phosphate pathway (PPP), in which glucose-6-phosphate becomes partially oxidized to generate NADPH and ribose-5-phosphate – a structural component of nucleotides.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“By converting excess pyruvate to lactate, proliferating cells prevent accumulation of cytosolic NADH and reduce ATP production promoting continued cytosolic glucose metabolism free from feedback repression by excess mitochondrial ATP generation.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The key enzymes in the pathway, transketolase-like 1 (TKTL1) and transaldolase (TALDO) are frequently overexpressed in cancer”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Wang et al., 2011a
- Not checked yetcites Xu et al., 2009b
Strength:plain· not yet calibratedCausal:correlational· 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
“This step is regulated by pyruvate kinase (PK), an enzyme that converts phosphoenolpyruvate to the final product of glycolysis, pyruvate.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
“Any excess glycolytic flux not utilized for biosynthesis is preferentially converted to lactate to help preserve a sufficient pool of NAD+ to sustain glycolysis and avoid flooding the mitochondria with a supply of NADH that would suppress the TCA cycle.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“To this end, ROS act as inhibitors of protein phosphatases such as PTEN and PTP1B, as well as activators of Src family kinases and MAPK (Denu and Tanner, 1998; Kamata et al., 2005; Lee et al., 2002; Yan and Berton, 1996).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Denu and Tanner, 1998
- Not checked yetcites Kamata et al., 2005 source
- Not checked yetcites Lee et al., 2002
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
“DHAP is converted by glycerol-3-phosphate dehydrogenase 1 (GPD1) into glycerol-3-phosphate, which is utilized in the biosynthesis of diverse phospholipids, a major structural component of cellular membranes.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
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
“wild-type, but not the mutant, p53 inhibits PPP by directly binding and inactivating the rate-limiting PPP enzyme glucose-6-phosphate dehydrogenase (G6PD)”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Jiang et al., 2011
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Thus, PKM2 is inhibited by tyrosine phosphorylation and activated by serine (Chaneton et al., 2012; Christofk et al., 2008b; Ye et al., 2012).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Chaneton et al., 2012
- Not checked yetcites Christofk et al., 2008b
- Not checked yetcites Ye et al., 2012
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“While PKM1 is more efficient at producing pyruvate, the majority of proliferating cells and essentially all cancer cells express primarily the PKM2 variant”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Christofk et al., 2008a
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Though glycolysis is classically depicted as a single chain of molecular events that leads to the generation of pyruvate, a number of glycolytic intermediates can be diverted into branching pathways, generating diverse biosynthetic precursors.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Through the generation of N-acetylglucosamine (GlcNAc), a substrate for N- and O-linked glycosylation, the hexosamine pathway provides substrates for cellular glycosylation reactions as well as heparan sulfate and hyaluronic acid biosynthesis, potentiates receptor-mediated signaling and regulates the stability of select proteins, including c-myc”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Itkonen et al., 2013
- Not checked yetcites Spiro, 2002
- Not checked yetcites Wellen et al., 2010
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Among such populations are stem-like subclones that emerge following the oncogene ablation in vivo, as well as circulating tumor cells (CTCs) (LeBleu et al., 2014; Viale et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites LeBleu et al., 2014
- Not checked yetcites Viale et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In support of this paradigm, a reintroduction of the PKM1 isoform compromises cancer cell proliferation and tumorigenesis in vivo, in part by negatively affecting serine-dependent biosynthesis (Ye et al., 2012).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Ye et al., 2012
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“while the acetyl-CoA serves as a precursor for lipid biosynthesis and protein acetylation.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Thus, c-myc not only facilitates glutamine uptake, but also promotes its utilization in the biogenesis of purine and pyrimidine bases.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, activity of CAD enzyme is regulated via phosphorylation by MAPK and by mTORC1-dependent S6 kinase (Ben-Sahra et al., 2013; Graves et al., 2000; Robitaille et al., 2013).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
What the sources say
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
“A non-essential amino acid containing two atoms of reduced nitrogen, glutamine serves as the principal way in which reduced nitrogen is transported between cells in metazoan organisms.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Load-bearingStrength:plain· not yet calibratedTests✓ 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.
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
“Thus, one glutamine molecule is used in the production of uracil and thymine, cytosine and adenine each require two, and building a guanine base costs a cell three molecules of glutamine.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“In addition to being utilized for nucleotide biosynthesis, glutamine can be directly deamidated to glutamate by glutaminase which is frequently upregulated in cancer cells in a c-myc-dependent manner.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
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.
None of the sources cited for this claim have been checked yet.
In the paper
“ASNS is frequently upregulated in tumors and is associated with poor prognosis (Sircar et al., 2012; Zhang et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
What the sources say
- Not checked yetcites Sircar et al., 2012
- Not checked yetcites Zhang et al., 2014 source
Strength:plain· not yet calibratedCausal:correlational· 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
“Imported acetate is converted to acetyl-CoA in a reaction catalyzed by acetyl-CoA synthetase 2 (ACSS2), which is a target for amplification in breast cancer.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In fact, all three major components involved in fatty acyl chain biosynthesis – ACLY, ACC and FASN – are frequently upregulated in transformed cells; furthermore, their inhibition reduces tumor cell growth in vitro and in vivo (Chajes et al., 2006; Flavin et al., 2010; Migita et al., 2008; Milgraum et al., 1997).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“These reports highlight that the cell lineage context, as well as potential secondary effects associated with the adaptation of cells to tissue culture conditions may play an important role in the choice of an anaplerotic substrate.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In a process referred to as reductive carboxylation, a section of the TCA cycle reverses itself, converting α-ketoglutarate into citrate, which can be then used to generate a source of cytosolic acetyl-CoA (Metallo et al., 2012; Wise et al., 2011).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Glutamine can be captured in mitochondria by glutaminase and the resulting glutamate converted into α-ketoglutarate by either glutamate dehydrogenase or amino acid transaminases.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“An increased capacity for the producing lipids de novo not only facilitates the formation of lipid bilayers, but also enables a cell to alter its membrane composition in favor of oxidative damage-resistant saturated fatty acids as means of adapting to oxidative stress (Rysman et al., 2010).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Rysman et al., 2010
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“A carrier of four nitrogen atoms, arginine serves as a precursor for a wide variety of nitrogenous compounds, among which are polyamines, creatine, agmatine and pyrroline-5-carboxylate, a precursor for the biosynthesis of proline.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Moreover, PC inhibition in NSCLC-derived cell lines suppresses fatty acid biosynthesis and dramatically reduces proliferation even in the presence of ample glutamine (Sellers et al., 2015).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
- Not checked yetcites Sellers et al., 2015
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Thus, hypoxia-associated deficit of acetyl-CoA can be augmented not only through the reductive carboxylation of α-ketoglutarate, but also by increasing the utilization of free acetate from plasma and interstitial fluid.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In c-myc-transformed cells in particular, glutamine deprivation leads to the collapse of the TCA cycle and triggers cell death, which can be rescued by the addition of oxaloacetate or a membrane-permeable form of α-ketoglutarate (Wise et al., 2008; Yuneva et al., 2007).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > USE OF GLYCOLYSIS/TCA CYCLE INTERMEDIATES FOR BIOSYNTHESIS AND NADPH PRODUCTION
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Polyamine levels increase in proliferating cells; moreover, polyamines have been shown to inhibit apoptosis and promote tumor growth and invasion (Casero and Marton, 2007; Gerner and Meyskens, 2004).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
What the sources say
- Not checked yetcites Casero and Marton, 2007
- Not checked yetcites Gerner and Meyskens, 2004
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“One possibility is that the inactivation of ASL and ASS1 allows cancer cells to accumulate ornithine, which is then utilized in the production of polyamines, a class of nitrogen-containing polycationic aliphatic carbon molecules.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“For instance, sirtuins, a class of deacetylases that catalyze the removal of acetyl marks from histone and non-histone proteins, utilize NAD+ as a cofactor, while FAD serves as a cofactor for a lysine-specific demethylase LSD1 (Imai et al., 2000; Shi et al., 2004).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Reciprocally, proline oxidase (POX), which mediates proline degradation, is negatively controlled by c-myc via miR-23b, and is a p53 target as well (Donald et al., 2001; Liu et al., 2012).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
What the sources say
- Not checked yetcites Donald et al., 2001
- Not checked yetcites Liu et al., 2012
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
“Among α-ketoglutarate-dependent dioxygenases are a TET family of DNA demethylases, Jumonji C family of histone demethylases, mRNA demethylases FTO and ALKBH5, and a family of prolyl hydroxylase (PHD) enzymes, which, among other processes, regulate HIF1α levels in response to oxygen availability and oxidative stress.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Argininosuccinate, in turn, is produced by the enzyme argininosuccinate synthase (ASS1) from citrulline and aspartate.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“SAM is a product of the one-carbon metabolic pathway and is fueled by serine catabolism as described above.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Tumors that exhibit SDH- and FH loss share a number of phenotypic features that are consistent with dioxygenase inhibition, among which is a characteristic global increase in DNA methylation (Killian et al., 2013; Letouze et al., 2013; Xiao et al., 2012), as well as elevated levels of HIF1α (Selak et al., 2005).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Proline can be produced either from glutamate or from arginine-derived ornithine via a common intermediate, pyrroline-5-carboxylate.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Indeed, withdrawal and readdition of glucose, as well as activation of oncogenic signaling via introduction of an oncogenic KRAS mutant or a constitutively active form of Akt, increase total histone acetylation, which, in turn, promotes the enhanced and broader gene expression (Lee et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
- Not checked yetcites Lee et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“The de novo biosynthesis of arginine is an integral part of the urea cycle, where it is derived from argininosuccinate in a cleavage reaction catalyzed by argininosuccinate lyase (ASL).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > INCREASED DEMAND FOR NITROGEN
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. 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
“The deposition of acetyl marks on histones is associated with the increased accessibility of the genomic DNA for the assembly of transcriptional complexes, and has a rapid turnover rate.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“As discussed earlier, tumors are often faced with nutrient- and oxygen-poor surroundings and develop various nutrient-scavenging strategies to bypass these limitations.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Furthermore, hypoxia impedes the ability of cells to carry out oxidative phosphorylation and other reactions that require oxygen and disrupts the redox balance, affecting cellular signaling and transcriptional programs.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“a gasotransmitter with complex and not yet fully defined functions in cellular physiology, among which are protection from oxidative stress, increased mitochondrial respiration, protection from apoptosis and facilitation of angiogenesis (Wu et al., 2015).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
What the sources say
- Not checked yetcites Wu et al., 2015
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
“Oncogene-driven metabolic reprogramming allows cancer cells to maintain deregulated proliferation, withstand metabolic challenges that are associated with oxygen and nutrient limitations, maintain a dedifferentiated state through alterations in global patterns of gene expression, and corrupt the surrounding microenvironment into actively assisting tumor growth and dissemination.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased extracellular acidification stimulates the proteolytic activity of matrix metalloproteinases (MMPs) and cathepsins, promoting the degradation of the extracellular matrix components and enhancing tumor invasion (Martinez-Zaguilan et al., 1996; Rothberg et al., 2013).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Martinez-Zaguilan et al., 1996
- Not checked yetcites Rothberg et al., 2013
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Thus, cancer cells upregulate the uptake of cysteine via the transcriptional upregulation of the xCT transporter, as well as secondary to the increased rate of glutamine utilization by cells (Lo et al., 2008).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
What the sources say
- Not checked yetcites Lo et al., 2008
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Thus, lactate promotes the stabilization of HIF1α and activates NF-κB and PI-3 kinase signaling in endothelial cells, as well as induces secretion of a pro-angiogenic factor VEGF from tumor-associated stromal cells (Constant et al., 2000; Schmid et al., 2007; Sonveaux et al., 2012; Vegran et al., 2011).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Constant et al., 2000 source
- Not checked yetcites Schmid et al., 2007
- Not checked yetcites Sonveaux et al., 2012
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“How cancer cells reprogram their microenvironment to assist tumor growth and dissemination is an area of intense investigation, but it is clear that such reprogramming encompasses multiple strategies, among which are secreted growth factors and alterations to the extracellular matrix and cell-cell interactions.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
Strength:boosted· 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
“In addition, a specific increase in the L enantiomer of 2-HG, which was shown to exert similar, but not identical, inhibitory effects on α-ketoglutarate-dependent dioxygenases was found in clear cell renal cell carcinoma, where it correlates with increased methylcytosine levels (Shim et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
- Not checked yetcites Shim et al., 2014 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased choline uptake is observed in breast and prostate cancer; in fact, radioactive 18F- and 11C-choline is used in the clinic for PET-based tumor imaging (Krause et al., 2013; Kwee et al., 2007).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
What the sources say
- Not checked yetcites Krause et al., 2013
- Not checked yetcites Kwee et al., 2007
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In various cellular settings, ectopic expression of a mutant IDH allele or treatment with exogenous D-2-HG is sufficient to induce DNA and histone hypermethylation and block cellular differentiation (Losman et al., 2013; Lu et al., 2012).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
- Not checked yetcites Losman et al., 2013 source
- Not checked yetcites Lu et al., 2012
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Increased levels of lactate also stimulate hyaluronic acid production by fibroblasts, which may contribute to tumor invasiveness (Stern et al., 2002).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Stern et al., 2002
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Specifically, numerous solid tumor types overexpress tryptophan-degrading dioxygenases indoleamine-2, 3-dioxygenase (IDO1) and tryptophan-2, 3-dioxygenase (TDO2), which catalyze the conversion of an essential amino acid, tryptophan, into its derivative, kynurenine (Munn and Mellor, 2007).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Munn and Mellor, 2007
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased lactate levels promote the emergence of an immune-permissive microenvironment by attenuating dendritic and T cell activation and monocyte migration (Fischer et al., 2007; Goetze et al., 2011; Gottfried et al., 2006).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, lactate stimulates the polarization of resident macrophages to a so-called M2 state, which plays a role in immunosuppression and wound healing (Carmona-Fontaine et al., 2013; Colegio et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Carmona-Fontaine et al., 2013
- Not checked yetcites Colegio et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Finally, kynurenine potentiates autocrine signaling through AhR on cancer cells themselves, promoting the degradation of the extracellular matrix and invasion (Opitz et al., 2011).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Opitz et al., 2011
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“While most of the studies to this point have been focused on alterations in the metabolism of glucose and glutamine, cancer cells utilize a great variety of other nutrients, among which are sulfur–containing amino acids cysteine and methionine, essential fatty acids, choline, trace metals, and vitamins.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“IDH mutations in AML are mutually exclusive with inactivating mutations in TET2 methylcytosine hydroxylases, further implicating mutant IDH as a bona fide driver of epigenetic remodeling (Figueroa et al., 2010).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > ALTERATIONS IN METABOLITE-DRIVEN GENE REGULATION
What the sources say
- Not checked yetcites Figueroa et al., 2010 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In a manner that is dependent on AhR, kynurenine promotes regulatory T-cell phenotype, further contributing to the suppression of antitumor immune responses (Fallarino et al., 2006).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > METABOLIC INTERACTIONS WITH THE MICROENVIRONMENT
What the sources say
- Not checked yetcites Fallarino et al., 2006
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“Micronutrients are utilized as cofactors for various enzymes and play complex and not yet fully defined roles in regulating cellular metabolic circuits, as well as signal transduction.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
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
“Interestingly, copper was recently shown to be required for BRAFV600E-driven ERK activation in melanoma cells, and the effect of copper depletion could be rescued by the constitutive activation of ERK (Brady et al., 2014).”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
What the sources say
- Not checked yetcites Brady et al., 2014
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
“As many cancers are characterized by increased methylation of CpG islands, alterations in ascorbic acid import may thus affect their epigenetic state as well.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ 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
“For instance, ascorbic acid acts as a cofactor for the α-ketoglutarate-dependent dioxygenases.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Most tumors display several of the six metabolic hallmarks, while few display all six.
“While few tumors display all six hallmarks, most display several.”
The paper relies on this without support.
Findings from animal models about dietary methyl donors and epigenetic marks apply to human tumorigenesis.
“Furthermore, diets deficient in choline and betaine were shown to directly affect histone and DNA methylation in a number animal models (Du et al., 2009; Mehedint et al., 2010; Niculescu et al., 2006), suggesting that alterations in exogenous methyl donor availability may have strong effects on cellular epigenetic state and thus contribute to tumorigenesis.”
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?
In the citing paper
“Even TCA cycle intermediates are not solely used to produce NADH for mitochondrial respiration, but intermediates can also be used to form nonessential amino acids and fatty acids, which facilitate protein synthesis, membrane construction and cholesterol synthesis (206).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [206]
In the citing paper
“The PPP is chiefly used for NADPH and ribose synthesis to produce nucleotides (206).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [206]
In the citing paper
“However, not all tumors are glutamine dependent because some tumors and embryonic stem cells are capable of proliferation without an exogenous supply of glutamine, because they can synthesize it (206).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [206]
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Flagged first, then by citations
12 of the 254 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Metabolic regulation of gene expression by histone lactylation
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Fundamentals of Cancer Metabolism
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“Because some altered metabolic features are observed quite generally across many types of cancer cells, reprogrammed metabolism is considered a hallmark of cancer (1, 2).”
BackgroundMetabolic reprogramming and cancer progression
Faubert, B., Solmonson, A., & DeBerardinis, R. J. (2020) · Science · doi:10.1126/science.aaw5473 · Cited by 2,740
“A central concept in cancer metabolism is that malignant cells acquire an enhanced ability to feed themselves by activating nutrient uptake mechanisms (33).”
BackgroundCystine transporter SLC7A11/xCT in cancer: ferroptosis, nutrient dependency, and cancer therapy
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Metadata
- Authors
- Pavlova, N. N., & Thompson, C. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Thompson, Craig B.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2016-01
- Volume
- 23
- Issue
- 1
- Pages
- 27-47
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC4715268
- OpenAlex
- W2234115940
- Semantic Scholar
- 1e8b6414a84ad7a310eeee976435e51a609d3979
- Cited by
- 5,926
- References
- 254
- Citations by year
- 2026: 576 · 2025: 556 · 2024: 661 · 2023: 678 · 2022: 819 · 2021: 846 · 2020: 601 · 2019: 477 · 2018: 352 · 2017: 252 · 2016: 103
- FWCI
- 36.25
- 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, 377 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
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute
- Terri Brodeur Breast Cancer Foundation
- National Institutes of Health
- 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, carcinogenesis, glucose uptake, amino acid uptake, nutrient acquisition, glycolysis, TCA cycle intermediates, NADPH production, nitrogen requirements, tumor microenvironment, tumor classification
- MeSH terms
- Animals, Antineoplastic Agents, Biological Transport, Cell Transformation, Neoplastic, Energy Metabolism, Humans, Mutation, Neoplasms, Signal Transduction, Metabolic Networks and Pathways
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 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (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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