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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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.
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Claims the paper makes
163 Not checked yet · 73 No basis given · 48 Own interpretation · 1 Sources not found
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
plaindirect- Asserted: passes — The authors put it forward as true.
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In 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
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In 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
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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
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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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
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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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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-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
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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
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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
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Probably 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
plain- Asserted: passes — The authors put it forward as true.
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Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“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
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plain- Asserted: passes — The authors put it forward as true.
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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
“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
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These 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
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It 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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“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
plain- Asserted: passes — The authors put it forward as true.
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Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“For instance, ascorbic acid acts as a cofactor for the α-ketoglutarate-dependent dioxygenases.”
§ THE EMERGING HALLMARKS OF CANCER METABOLISM > REMAINING QUESTIONS
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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]
Citations
Cites
Hanahan, D., & Weinberg, R. A. (2000) · Cell · doi:10.1016/s0092-8674(00)81683-9 · Cited by 29,219
Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
Li, Y., Jiang, Q. L., Cao, G.-F., Yao, J., & Yan, B. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373980 · Cited by 16,351
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-citationWarburg, O. (1956) · Science · doi:10.1126/science.123.3191.309 · Cited by 13,425
An Integrated Genomic Analysis of Human Glioblastoma Multiforme
Parsons, D. W., Jones, S., Zhang, X., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Siu, I.-M., Gallia, G. L., et al. (2008) · Science · doi:10.1126/science.1164382 · Cited by 5,857
Accessories to the Crime: Functions of Cells Recruited to the Tumor Microenvironment
Hanahan, D., & Coussens, L. M. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.02.022 · Cited by 4,632
The metabolism of tumors in the body
Warburg, O., Wind, F., & Negelein, E. (1927) · Journal of General Physiology · doi:10.1085/jgp.8.6.519 · Cited by 4,416
Cancer genes and the pathways they control
Vogelstein, B., & Kinzler, K. W. (2004) · Nature Medicine · doi:10.1038/nm1087 · Cited by 4,346
Cancer-associated IDH1 mutations produce 2-hydroxyglutarate
Dang, L., White, D. W., Gross, S., Bennett, B. D., Bittinger, M. A., Driggers, E. M., Fantin, V. R., Jang, H. G., Jin, S., Keenan, M. C., et al. (2009) · Nature · doi:10.1038/nature08617 · Cited by 4,154
Self-citationHistone demethylation mediated by the nuclear amine oxidase homolog LSD1
Shi, Y., Lan, F., Matson, C., Mulligan, P., Whetstine, J. R., Cole, P. A., Casero, R. A., & Shi, Y. (2004) · Cell · doi:10.1016/j.cell.2004.12.012 · Cited by 4,051
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Items 501–600 of 1,029
Hyperglycemia exacerbates colon cancer malignancy through hexosamine biosynthetic pathway
Vasconcelos-dos-Santos, A., Loponte, H. F. B. R., Mantuano, N. R., Oliveira, I. D. A., Paula, I. F. D., Teixeira, L. K., de‐Freitas‐Junior, J. C. M., Gondim, K. C., Heise, N., Mohana‐Borges, R., et al. (2017) · Oncogenesis · doi:10.1038/oncsis.2017.2 · Cited by 120
Hepatic Tumor Microenvironments and Effects on NK Cell Phenotype and Function
Fernández, J. P., Luddy, K. A., Harmon, C., & O’Farrelly, C. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20174131 · Cited by 119
“In oxygen-poor environments and transformed cells, a large portion of pyruvate is converted to lactate by lactate dehydrogenase [67].”
BackgroundCong, V. T., Houng, J. L., Kavallaris, M., Chen, X., Tilley, R. D., & Gooding, J. J. (2022) · Chemical Society Reviews · doi:10.1039/d1cs00707f · Cited by 129
Mitophagy: A novel perspective for insighting into cancer and cancer treatment
Song, C., Pan, S., Zhang, J., Li, N., & Geng, Q. (2022) · Cell Proliferation · doi:10.1111/cpr.13327 · Cited by 120
“The expression and activity of key enzymes during glycolysis of cancer cells can obviously affect this metabolic process.(131,132) It was reported for p62/SQSTM1-dependent mitophagy to selectively degrade hexokinase 2 (HK2) to control glycolytic levels.”
BackgroundWei, S., Zhang, J., Zhao, R., Shi, R., An, L., Yu, Z., Zhang, Q., Zhang, J., Yao, Y., Li, H., et al. (2024) · Cell Death Discovery · doi:10.1038/s41420-024-01898-4 · Cited by 145
Targeting ATP-Citrate Lyase in Hyperlipidemia and Metabolic Disorders
Pinkosky, S. L., Groot, P. H. E., Lalwani, N. D., & Steinberg, G. R. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.09.001 · Cited by 118
Fuhr, L., El‐Athman, R., Scrima, R., Cela, O., Carbone, A., Knoop, H., Li, Y., Hoffmann, K., Laukkanen, M. O., Corcione, F., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.07.002 · Cited by 123
“Cancer cells are known to have a reprogrammedmetabolism [9,51,59], which allows them to fulfil the enhanced energy demands commonly leading to a switch towards hypoxic glycolysis over normoxic glycolysis.”
BackgroundZhan, Q., Yi, K., Cui, X., Li, X., Yang, S., Wang, Q., Fang, C., Tan, Y., Li, L., Xu, C., et al. (2022) · Neuro-Oncology · doi:10.1093/neuonc/noac071 · Cited by 103
Kosti, A., Araujo, P. R. D., Li, W.-Q., Guardia, G. D. A., Chiou, J., Yi, C., Ray, D., Meliso, F. M., Li, Y.-M., Delambre, T., et al. (2020) · Genome biology · doi:10.1186/s13059-020-02115-y · Cited by 115
Modulation of endothelium function by fatty acids
Mallick, R., & Duttaroy, A. K. (2021) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-021-04260-9 · Cited by 129
Zapata, L., Pich, O., Serrano, L. G., Kondrashov, F. A., Ossowski, S., & Schaefer, M. H. (2018) · Genome biology · doi:10.1186/s13059-018-1434-0 · Cited by 110
Quanz, M., Bender, E., Kopitz, C., Grünewald, S., Schlicker, A., Schwede, W., Eheim, A. L., Toschi, L., Neuhaus, R., Richter, C., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-1253 · Cited by 117
“Tumorigenesis is associated with profound reprogramming of cellular metabolism, and numerous connections of oncogenic drivers and cancer cell metabolism have been described (1, 2).”
BackgroundSun, K., Zhang, X., Shi, J., Huang, J., Wang, S., Li, X., Lin, H., Zhao, D., Ye, M., Zhang, S., et al. (2025) · Journal of Clinical Investigation · doi:10.1172/jci187024 · Cited by 138
Macropinocytosis, mTORC1 and cellular growth control
Yoshida, S., Pacitto, R., Inoki, K., & Swanson, J. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2710-y · Cited by 114
“Thus, macropinocytosis-mediated ingestion of extracellular protein is now considered a hallmark of cancer metabolism [121].”
BackgroundMetabolic functions of macropinocytosis
Palm, W. (2018) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2018.0285 · Cited by 115
Metabolic gene alterations impact the clinical aggressiveness and drug responses of 32 human cancers
Sinkala, M., Mulder, N., & Martin, D. P. (2019) · Communications Biology · doi:10.1038/s42003-019-0666-1 · Cited by 111
Du, W., Gu, M., Hu, M., Pinchi, P., Chen, W., Ryan, M., Nold, T. M., Bannaga, A., & Xu, H. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109848 · Cited by 122
“Cancer cells, due to their high metabolism and fast turnover of metal-binding macromolecules, tend to accumulate heavy metal ions in endolysosomal compartments (Chandler et al., 2016; Kroemer and Jäättelä, 2005; Pavlova and Thompson, 2016).”
Backgroundvon der Heide, E. K., Neumann, M., Vosberg, S., James, A. R., Schroeder, M. P., Ortiz-Tánchez, J., Isaakidis, K., Schlee, C., Luther, M., Jöhrens, K., et al. (2016) · Leukemia · doi:10.1038/leu.2016.324 · Cited by 114
Naz, S., Sowers, A. L., Choudhuri, R., Wissler, M. F., Gamson, J., Mathias, A., Cook, J. A., & Mitchell, J. B. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-3575 · Cited by 113
“Abemaciclib alters NSCLC metabolism by disrupting key nutrient sensing pathways In recent years, it has been well appreciated that cancer cells have the ability to rewire theirmetabolism and energy production networks in response to altered microenvironment conditions to support rapid proliferation, invasion,metastasi…”
BackgroundThe roles of sirtuins family in cell metabolism during tumor development
Zhu, S., Dong, Z., Ke, X., Hou, J., Zhao, E., Zhang, K., Wang, F., Yang, L., Xiang, Z., & Cui, H. (2018) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2018.11.003 · Cited by 113
Skp2 dictates cell cycle-dependent metabolic oscillation between glycolysis and TCA cycle
Liu, J., Peng, Y., Shi, L., Wan, L., Inuzuka, H., Long, J., Guo, J., Zhang, J., Yuan, M., Zhang, S., et al. (2020) · Cell Research · doi:10.1038/s41422-020-0372-z · Cited by 117
“This may be in part due to ATP needs, as cells rely mostly on the TCA cycle during G1 phase while switching to glycolysis, a less economic form of ATP production, to accumulate intermediate metabolites that are used as building blocks to synthesize biomacromolecules for subsequent DNA replication and cytokinesis.(19)…”
BackgroundYu, T., Ma, D., Liu, Y., Xiao, Y., Gong, Y., Jiang, Y., Shao, Z.-M., Hu, X., & Di, G. (2021) · Molecular Therapy · doi:10.1016/j.ymthe.2021.03.003 · Cited by 113
Circadian regulation of cancer cell and tumor microenvironment crosstalk
Xuan, W., Khan, F., James, C. D., Heimberger, A. B., Lesniak, M. S., & Chen, P. (2021) · Trends in Cell Biology · doi:10.1016/j.tcb.2021.06.008 · Cited by 113
“…and progression via the regulation of multiple cancer hallmarks in cancer cells [29,30], which include the DNA damage response, apoptosis, cell cycle, and senescence [1,18,31,32], proliferation [1,2], metabolism [30,33,34], replicative immortality [35], and genome instability and mutation [34].”
BackgroundLangevin, S. M., Kuhnell, D., Parry, T. L., Biesiada, J., Huang, S., Wise-Draper, T. M., Casper, K. A., Zhang, X., Medvedovic, M., & Kasper, S. (2017) · Oncotarget · doi:10.18632/oncotarget.19614 · Cited by 107
“Malignant cells, including HNSCC [37], have a voracious appetite for glucose and glutamine, which are required to support their high energy and biosynthesis demands due to a predilection for aerobic glycolysis [38, 39].”
BackgroundCancer cell metabolic reprogramming: a keystone for the response to immunotherapy
Cerezo, M., & Rocchi, S. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-03175-5 · Cited by 118
Interplay Among Metabolism, Epigenetic Modifications, and Gene Expression in Cancer
Huo, M., Zhang, J., Huang, W., & Wang, Y. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.793428 · Cited by 117
“The metabolic reprogramming of tumor cells enables them to obtain essential nutrients from a nutrition-deficient environment to maintain continuous cell growth and proliferation (Pavlova and Thompson, 2016).”
BackgroundLi, Y., Fahrmann, J. F., Aftabizadeh, M., Zhao, Q., Tripathi, S. C., Zhang, C., Yuan, Y., Ann, D. K., Hanash, S., & Yu, H. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.110870 · Cited by 116
Oxidative stress and hypoxia in normal and leukemic stem cells
Testa, U., Labbaye, C., Castelli, G., & Pelosi, E. (2016) · Experimental Hematology · doi:10.1016/j.exphem.2016.04.012 · Cited by 118
PGC-1 Coactivators: Shepherding the Mitochondrial Biogenesis of Tumors
Luo, C., Widlund, H. R., & Puigserver, P. (2016) · Trends in cancer · doi:10.1016/j.trecan.2016.09.006 · Cited by 110
“An Emerging Role of PGC-1 Coactivators in Cancer Metabolism Metabolic reprogramming represents one of the hallmarks of human cancers [1,2], a concept first recognized by Otto Warburg and based on observations that glycolytic fermentation in cancer cells persists even in the presence of sufficient oxygen.”
Chen, Z., Zuo, X., Zhang, Y., Han, G., Zhang, L., Wu, J., & Wang, X. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-0616-8 · Cited by 111
Energy balance and gastrointestinal cancer: risk, interventions, outcomes and mechanisms
Ulrich, C. M., Himbert, C., Holowatyj, A. N., & Hursting, S. D. (2018) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-018-0053-2 · Cited by 111
The Pleiotropic Effects of Glutamine Metabolism in Cancer
Bott, A. J., Maimouni, S., & Zong, W. (2019) · Cancers · doi:10.3390/cancers11060770 · Cited by 111
“Production of UDP-GlcNAc and O-GlcNAcylation are emerging as a means to link nutrient levels to intracellular functions [67,69,70], and has been implicated in regulating intracellular signaling which impact tumorigenesis [71,72].”
BackgroundBranched-chain amino acids sustain pancreatic cancer growth by regulating lipid metabolism
Lee, J. H., Cho, Y.-R., Kim, J. H., Kim, J.-W., Nam, H. Y., Kim, S. W., & Son, J. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0350-z · Cited by 111
Drury, J., Rychahou, P. G., He, D., Jafari, N., Wang, C., Lee, E. Y., Weiss, H. L., Evers, B. M., & Zaytseva, Y. Y. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.01185 · Cited by 111
Recent advances in heat shock proteins in cancer diagnosis, prognosis, metabolism and treatment
Yang, S., Xiao, H., & Cao, L. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.112074 · Cited by 115
Current and future perspectives of functional metabolomics in disease studies–A review
Yan, M., & Xu, G. (2018) · Analytica Chimica Acta · doi:10.1016/j.aca.2018.04.006 · Cited by 105
Colvin, H. S., Nishida, N., Konno, M., Haraguchi, N., Takahashi, H., Nishimura, J., Hata, T., Kawamoto, K., Asai, A., Tsunekuni, K., et al. (2016) · Scientific Reports · doi:10.1038/srep36289 · Cited by 111
O-GlcNAcylation of RACK1 promotes hepatocellular carcinogenesis
Duan, F., Wu, H., Jia, D., et al. (2018) · Journal of Hepatology · doi:10.1016/j.jhep.2018.02.003 · Cited by 109
“As a consequence of glucose metabolism in cancer cells through aerobic glycolysis[27] and hexosamine biosynthesis[28], we found that RACK1 mutated cells displayed less release of lactate”
BackgroundHumanized mouse models of immunological diseases and precision medicine
Shultz, L. D., Keck, J., Burzenski, L. M., Jangalwe, S., Vaidya, S., Greiner, D. L., & Brehm, M. A. (2019) · Mammalian Genome · doi:10.1007/s00335-019-09796-2 · Cited by 116
Size-Tunable Assemblies Based on Ferrocene-Containing DNA Polymers for Spatially Uniform Penetration
Tan, J., Li, H., Hu, X., Abdullah, R., Xie, S., Zhang, L., Zhao, M., Luo, Q., Li, Y., Sun, Z., et al. (2019) · Chem · doi:10.1016/j.chempr.2019.05.024 · Cited by 109
Mitochondrial metabolism-mediated redox regulation in cancer progression
Boese, A. C., & Kang, S. (2021) · Redox Biology · doi:10.1016/j.redox.2021.101870 · Cited by 114
“are still being actively researched, the Warburg effect has been demonstrated to benefit proliferative cancer cells through rapid ATP generation and simultaneous flux through the pentose phosphate pathway (PPP) to support redox homeostasis and biosynthesis [2].”
BackgroundHuang, K., Han, Y., Chen, Y., Shen, H., Zeng, S., & Cai, C. (2025) · Molecular Cancer · doi:10.1186/s12943-024-02205-6 · Cited by 121
Singleton, K. R., Crawford, L. A., Tsui, E. L., Manchester, H. E., Maertens, O., Liu, X., Liberti, M. V., Magpusao, A. N., Stein, E. M., Tingley, J. P., et al. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.11.022 · Cited by 102
“Of note were alterations in glycolysis, serine, and glutamine metabolism, each of which has been implicated in MYC-driven oncogenesis (Jin et al., 2016; Pavlova and Thompson, 2016; Stine et al., 2015).”
BackgroundYousuf, M., Shamsi, A., Κhan, P., Shahbaaz, M., Alajmi, M. F., Hussain, A., Hasan, G. M., Islam, A., Haque, Q. M. R., & Hassan, M. I. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21103526 · Cited by 109
“Thus, the identification of a selective CDK-6 inhibitor may be used as therapeutic targeting of cancer cell growth and metabolic alterations [2,9].”
BackgroundChen, X., Tang, G.-X., Luo, W.-H., Shao, W., Dai, J., Zeng, S.-T., Huang, Z., Chen, S.-B., & Tan, J. (2021) · Journal of the American Chemical Society · doi:10.1021/jacs.1c08860 · Cited by 109
Liver-Type Glutaminase GLS2 Is a Druggable Metabolic Node in Luminal-Subtype Breast Cancer
Lukey, M. J., Cluntun, A. A., Katt, W. P., Lin, M.-C. J., Druso, J. E., Ramachandran, S., Erickson, J. W., Le, H. H., Wang, Z.-E., Blank, B., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.08.076 · Cited by 103
“For example, most tumors exhibit elevated glucose uptake coupled to lactate secretion regardless of O 2 availability (the Warburg effect), and cancer cells also frequently depend on an exogenous supply of glutamine (Pavlova and Thompson, 2016).”
Wnt canonical pathway activates macropinocytosis and lysosomal degradation of extracellular proteins
Tejeda‐Muñoz, N., Albrecht, L. V., Bui, M. H., & Robertis, E. M. D. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1903506116 · Cited by 107
“Glycolytic metabolism is a well-known hallmark of cancer (59) and it is possible that macropinocytosis by Wnt pathway or Ras-activating mutations will contribute to this effect.”
BackgroundILF3 is a substrate of SPOP for regulating serine biosynthesis in colorectal cancer
Li, K., Wu, J., Qin, B., Fan, Z.-M., Tang, Q., Lu, W., Zhang, H., Xing, F., Meng, M., Zou, S., et al. (2019) · Cell Research · doi:10.1038/s41422-019-0257-1 · Cited by 107
Epigenomic Reprogramming as a Driver of Malignant Glioma
Phillips, R. E., Soshnev, A. A., & Allis, C. D. (2020) · Cancer Cell · doi:10.1016/j.ccell.2020.08.008 · Cited by 111
“IDHs are important metabolic enzymes which convert the TCA metabolite isocitrate into alpha-ketoglutarate (alpha-KG) (Pavlova and Thompson, 2016).”
BackgroundO-GlcNAcylation promotes pancreatic tumor growth by regulating malate dehydrogenase 1
Zhu, Q., Zhou, H., Wu, L., Lai, Z., Geng, D., Yang, W., Zhang, J., Fan, Z., Qin, W., Wang, Y., et al. (2022) · Nature Chemical Biology · doi:10.1038/s41589-022-01085-5 · Cited by 107
Mitochondrial DNA is a major source of driver mutations in cancer
Kim, M., Mahmood, M., Reznik, E., & Gammage, P. A. (2022) · Trends in cancer · doi:10.1016/j.trecan.2022.08.001 · Cited by 113
Cancer metabolites: promising biomarkers for cancer liquid biopsy
Wang, W., Rong, Z., Wang, G., Hou, Y., Yang, F., & Qiu, M. (2023) · Biomarker Research · doi:10.1186/s40364-023-00507-3 · Cited by 113
“In turn, tumor cells can alter metabolic fluxes and reprogram their metabolism to maintain their own biosynthesis and energy requirements within oncogenic mutations and tumour suppressor contexts [17, 18].”
BackgroundLi, B., Li, Y., Zhou, H., Xu, Y., Cao, Y., Cheng, C., Peng, J., Li, H., Zhang, L., Su, K., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000553 · Cited by 110
“[9] Cancer cells frequently exhibit alterations in FA metabolism to sustain growth and proliferation, fulfill energy requirements, provide cellular building blocks for membrane formation, and produce signaling molecules or post-translational modifications.”
BackgroundEffect of Mutant p53 Proteins on Glycolysis and Mitochondrial Metabolism
Eriksson, M., Ambroise, G., Ouchida, A. T., Queiroz, A. L., Smith, D. H., Giménez-Cassina, A., Iwanicki, M., Muller, P. A. J., Norberg, E., & Vakifahmetoglu-Norberg, H. (2017) · Molecular and Cellular Biology · doi:10.1128/mcb.00328-17 · Cited by 110
“Altered metabolism is a characteristic of cancer and a key contributor to tumor development (29).”
BackgroundThe role of Wnt signaling pathway in tumor metabolic reprogramming
Mo, Y., Wang, Y., Zhang, L., Yang, L., Zhou, M., Li, X., Li, Y., Li, G., Zeng, Z., Xiong, W., et al. (2019) · Journal of Cancer · doi:10.7150/jca.31166 · Cited by 106
“This abnormal metabolic change is called metabolic reprogramming of tumors [7-10].”
BackgroundStarve Cancer Cells of Glutamine: Break the Spell or Make a Hungry Monster?
Jiang, J., Srivastava, S., & Zhang, J. (2019) · Cancers · doi:10.3390/cancers11060804 · Cited by 108
Crosstalk of lncRNA and Cellular Metabolism and Their Regulatory Mechanism in Cancer
Lin, Y.-H. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21082947 · Cited by 103
“Cancer cells can reprogram cellular metabolism to adapt and survive in nutritionally restricted environments [1].”
BackgroundDecoding microglial immunometabolism: a new frontier in Alzheimer's disease research
Jung, E. S., Choi, H., & Mook-Jung, I. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00825-0 · Cited by 124
Genini, D., Brambilla, L., Laurini, E., Merulla, J., Civenni, G., Pandit, S., D'Antuono, R., Perez, L., Levy, D. E., Pricl, S., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1615730114 · Cited by 106
“Changes in mitochondrial dynamics and energy homeostasis are emerging as important elements in cancer (18, 19).”
BackgroundQian, Y., Wang, X., Li, Y., Cao, Y., & Chen, X. (2016) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-16-0118 · Cited by 107
“Our finding is also consistent with the recent classification of the opportunistic uptake of extracellular nutritional molecules as an emerging hallmark for cancer metabolism (39) and the contribution of macropinocytosis in the uptake of extracellular molecules in A549 lung cancer and pancreatic cancer (40, 41).”
BackgroundResultDunphy, M. P., Harding, J. J., Venneti, S., Zhang, H., Burnazi, E. M., Bromberg, J., Omuro, A. M. P., Hsieh, J. J.-D., Mellinghoff, I. K., Staton, K. D., et al. (2018) · Radiology · doi:10.1148/radiol.2017162610 · Cited by 107
Condelli, V., Crispo, F., Pietrafesa, M., Lettini, G., Matassa, D. S., Esposito, F., Landriscina, M., & Maddalena, F. (2019) · Cells · doi:10.3390/cells8060532 · Cited by 107
“Cancer cells are able to reprogram their metabolism so as to acquire and maintain malignant properties in order to adapt rapidly and survive in ever-changing environments [52,56,121,122].”
BackgroundQiu, P., Zhou, Y., Oyang, L., Wu, N., Tang, Y., Su, M., Luo, X., Wang, Y., Sheng, X., Ma, J., et al. (2021) · Molecular Therapy · doi:10.1016/j.ymthe.2021.11.010 · Cited by 109
Emerging roles of hnRNPA1 in modulating malignant transformation
Roy, R., Huang, Y., Seckl, M. J., & Pardo, O. E. (2017) · Wiley Interdisciplinary Reviews - RNA · doi:10.1002/wrna.1431 · Cited by 104
“The deregulation of cellular energetics is now a recognized hallmark of cancer, with cancer cells favoring aerobic glycolysis with associated changes to mitochondrial metabolism that better supports their biosynthetic needs.(123) Here, glucose metabolism is diverted from ATP production toward the synthesis of cellular…”
BackgroundNDRG1 regulates neutral lipid metabolism in breast cancer cells
Sevinsky, C. J., Khan, F., Kokabee, L., Darehshouri, A., Maddipati, K. R., & Conklin, D. S. (2018) · Breast Cancer Research · doi:10.1186/s13058-018-0980-4 · Cited by 103
“Lipid synthesis is linked with glycolysis, and is a required component of transformed cell physiology [58].”
BackgroundTargeting Tumor Metabolism with Plant-Derived Natural Products: Emerging Trends in Cancer Therapy
Guerra, Â. R., Duarte, M. F., & Duarte, I. F. (2018) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.8b04104 · Cited by 102
Dissecting the role of hyaluronan synthases in the tumor microenvironment
Passi, A. G., Vigetti, D., Buraschi, S., & Iozzo, R. V. (2019) · FEBS Journal · doi:10.1111/febs.14847 · Cited by 106
Epigenetic mechanisms and the hallmarks of cancer: an intimate affair.
Darwiche, N. (2020) · PubMed Central · Cited by 105
Deregulation of Lipid Metabolism: The Critical Factors in Ovarian Cancer
Ji, Z., Shen, Y., Feng, X., Kong, Y., Shao, Y. W., Meng, J., Zhang, X., & Yang, G. S. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.593017 · Cited by 103
“Lipid metabolism could be regulated by suppressing fatty acid synthesis, accelerating fatty acid degradation via oxidation, diverting fatty acid to storage, retarding fatty acid release from storage, and blocking fatty acids intake (23).”
BackgroundPlasticity of cancer invasion and energy metabolism
Parlani, M., Jorgez, C. J., & Friedl, P. (2022) · Trends in Cell Biology · doi:10.1016/j.tcb.2022.09.009 · Cited by 106
Hwang, C. Y., Choe, W., Yoon, K., Ha, J., Kim, S. S., Yeo, E., & Kang, I. (2022) · Nutrients · doi:10.3390/nu14224932 · Cited by 115
Metabolic recoding of epigenetics in cancer
Wang, Y., & Lei, Q. (2018) · 癌症:英文版 · doi:10.1186/s40880-018-0302-3 · Cited by 109
“Since the postulation of aerobic glycolysis (Warburg effect) in the early 20th century [1], metabolic reprogramming in cancer has been the subject of extensive research [2].”
BackgroundRegulatory roles of long noncoding RNAs implicated in cancer hallmarks
Wang, J., Zhang, X., Chen, W., Hu, X., Li, J., & Liu, C. (2019) · International Journal of Cancer · doi:10.1002/ijc.32277 · Cited by 102
“Compared to normal cells, cancer cells have distinct metabolic characteristics, such as excessive glucose uptake, higher dependence on aerobic glycolysis, increased glutamine uptake and glutaminolysis andmodified lipid metabolism.(168) Glucose is the primary energy source for cells.”
BackgroundGaroffolo, G., & Pesce, M. (2019) · Cells · doi:10.3390/cells8121607 · Cited by 105
“Findings obtained in tumor biology show hat there is an interplay between cell met bolism nd tumor microenvironment [50,51].”
BackgroundTCA Cycle Rewiring as Emerging Metabolic Signature of Hepatocellular Carcinoma
Todisco, S., Convertini, P., Iacobazzi, V., & Infantino, V. (2019) · Cancers · doi:10.3390/cancers12010068 · Cited by 105
“Consequently, NADH accumulation and chain respiratory alteration facilitate this conversion.”
BackgroundInfluentialBensimon, A., Pizzagalli, M. D., Kartnig, F., Dvorak, V., Essletzbichler, P., Winter, G. E., & Superti-Furga, G. (2020) · Cell Chemical Biology · doi:10.1016/j.chembiol.2020.04.003 · Cited by 102
Zhu, W., Wang, J., Liu, X., Yanbin, X., Zhai, R., Zhang, J., Wang, M., Wang, M., & Liu, L. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-05157-1 · Cited by 105
“In fact, mitochondrial function is critical for cancer development [10], and especially so for the viability of metastasized cells [42].”
BackgroundToyokuni, S. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.10.401 · Cited by 96
Ding, Y., Wang, H., Niu, J., Luo, M., Gou, Y., Miao, L., Zou, Z., & Cheng, Y. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17040558 · Cited by 101
“Cancer cells rewire their metabolism to survive and to promote proliferation, growth, and metastasis [6,7].”
BackgroundFang, G., Zhang, P., Liu, J., et al. (2019) · Cancer Letters · doi:10.1016/j.canlet.2019.08.003 · Cited by 102
Choi, H.-J., Jhe, Y.-L., Kim, J., Lim, J. Y., Lee, J. E., Shin, M., & Cheong, J. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101589 · Cited by 102
“In particular, to cope with the uncertainty in securing nutrients and appropriate energy substrates, CSCs harness OXPHOS as the dominant metabolic strategy, which is far more efficient than glycolysis but comes at a cost of overproduced ROS, thereby requiring large amounts of NADPH as a counteractive measure [23].”
BackgroundYAP/TAZ drives cell proliferation and tumour growth via a polyamine–eIF5A hypusination–LSD1 axis
Li, H., Wu, B.-K., Kanchwala, M., Cai, J., Wang, L., Xing, C., Zheng, Y., & Pan, D. (2022) · Nature Cell Biology · doi:10.1038/s41556-022-00848-5 · Cited by 106
“While most cancer metabolic studies have focused on metabolites that serve as building blocks or energy sources 1 , how oncogenic signaling controls metabolites that play regulatory roles in driving cell proliferation and tumor growth is less understood.”
InfluentialOf the many cellular responses activated by TP53, which ones are critical for tumour suppression?
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“Notably, certain cancer cells are able to acquire nutrients from nutrient-poor environments, thereby enabling their expansion while simultaneously impairing the function of neighbouring non-transformed cells, including T lymphocytes that might otherwise attack the malignant cells [103, 105].”
BackgroundEngineered extracellular vesicles as intelligent nanosystems for next-generation nanomedicine
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RNA m 1 A methylation regulates glycolysis of cancer cells through modulating ATP5D
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Regulatory mechanisms of one-carbon metabolism enzymes
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Disrupting glutamine metabolic pathways to sensitize gemcitabine-resistant pancreatic cancer
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GLUT1 protects prostate cancer cells from glucose deprivation-induced oxidative stress
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““aerobic glycolysis”), is employed to obtain NADPH as well as the required precursors for biosynthesis [3].”
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Targeting glutamine metabolism slows soft tissue sarcoma growth
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The Implications of PDK1–4 on Tumor Energy Metabolism, Aggressiveness and Therapy Resistance
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“Besides other hallmarks of cancer, such as sustained proliferative signaling, resistance to cell death, invasiveness and increased angiogenesis, tumors are characterized by their altered metabolic features (1, 2).”
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The Benefits and Safety of Monoclonal Antibodies: Implications for Cancer Immunotherapy
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Escaping Death: Mitochondrial Redox Homeostasis in Cancer Cells
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BackgroundThe Role of RNA Editing in Cancer Development and Metabolic Disorders
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“It is well-established that cancers often overcome unwanted stresses by hijacking metabolic pathways, and metabolic disorders like obesity and diabetes are strong predisposing factors to cancers (206, 207).”
BackgroundA Potential Role of YAP/TAZ in the Interplay Between Metastasis and Metabolic Alterations
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“Hence, cancer cells need to adapt their metabolism to these changes to develop tumors (2).”
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“and survive the environmental fluctuations in nutrient and oxygen availability when tumor growth exceeds the delivery capabilities of the existing blood vessels [2].”
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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
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