The DOI matches its Crossref record; 119 of the 122 references it cites were found in a registry or an index; none of the 65 sources its claims cite is checked for support yet.
Tumor suppressors and cell metabolism: a recipe for cancer growth
Open accessAbstract
Growing tumors face two major metabolic challenges—how to meet the bioenergetic and biosynthetic demands of increased cell proliferation, and how to survive environmental fluctuations in external nutrient and oxygen availability when tumor growth outpaces the delivery capabilities of the existing vasculature. Cancer cells display dramatically altered metabolic circuitry that appears to directly result from the oncogenic mutations selected during the tumorigenic process. An emerging theme in cancer biology is that many of the genes that can initiate tumorigenesis are intricately linked to metabolic regulation. In turn, it appears that a number of well-established tumor suppressors play critical roles in suppressing growth and/or proliferation when intracellular supplies of essential metabolites become reduced. In this review, we consider the potential role of tumor suppressors as metabolic regulators.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that oncogenic and tumor suppressor networks reprogram cancer cell metabolism to support growth and proliferation while also enabling adaptation to metabolic stress. It focuses on glycolysis, mitochondrial biosynthesis, AMPK, p53, HIF1, and autophagy as interconnected metabolic regulators in tumorigenesis.
Key findings
- Proliferating cancer cells shift to aerobic glycolysis; >90% of pyruvate from glucose is converted to lactate by LDH-A, while the remaining ~10% enters mitochondria for biosynthetic pathways.
- Tumor suppressors including p53, LKB1, TSC2, PTEN, VHL, SDH, FH, and Beclin-1 act as metabolic brakes or adaptation regulators, whereas oncogenes such as PI3K/Akt, c-Myc, and HIF1 promote nutrient uptake, glycolysis, biosynthesis, and survival.
- AMPK is activated by energetic stress via LKB1 and can phosphorylate p53 at Ser-15, inducing a metabolic cell cycle checkpoint; in the absence of p53, metformin treatment delays tumor progression in cited work.
- Autophagy is a conserved metabolic stress response and tumor suppressor mechanism; Beclin-1 haploinsufficiency promotes tumorigenesis in mouse models and is associated with breast and ovarian cancers in humans, and ~30% of cancers cannot be detected by FDG-PET.
Methods
- Narrative review with no primary experimental data; it synthesizes literature on tumor suppressors and cell metabolism.
- No sample, dataset, or statistical analysis is reported; the article cites 116 references.
- Main analysis is a conceptual synthesis of oncogene/tumor suppressor signaling, metabolic pathways, and therapeutic implications.
Limitations
- The paper states that it remains debated whether metabolic changes are a consequence or cause of tumorigenesis; the exact contribution of AMPK to tumor progression is unclear; the stimuli and target genes for p53-dependent metabolic responses remain to be determined; and the role of p53 in autophagy remains controversial.
- Evident: as a narrative review, it does not systematically search or quantitatively synthesize evidence, and many mechanistic claims rely on cited studies rather than new data.
- Evident: tumor heterogeneity and context dependence may limit generalizability; the paper notes that individual tumor cells could display distinct metabolic signatures and that ~30% of cancers are FDG-PET negative.
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Claims the paper makes
51 Own interpretation · 44 Not checked yet
In the paper
“tumor cells, in order to meet the increased requirements of proliferation, often display fundamental changes in pathways of energy metabolism and nutrient uptake (Garber 2006).”
What the sources say
- Not checked yetcites Garber 2006
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“tumor cells preferentially use glycolysis over mitochondrial oxidative phosphorylation (OXPHOS) for glucose-dependent ATP production even in the presence of ample oxygen to fuel mitochondrial respiration, a phenomenon known as the ''Warburg effect'' (Warburg 1956).”
- Also stated in: § Glycolysis-metabolic reprogramming fuels cell growth and proliferation · plain
“One of the primary metabolic changes associated with proliferating tumor cells is induction of aerobic glycolysis (Fig. 1).”
What the sources say
- Not checked yetcites Warburg 1956
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Glycolysis-metabolic reprogramming fuels cell growth and proliferation · plain
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
“supporting the theory that alterations in cellular metabolism may contribute to the malignant phenotype.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“AMPK appears to function across evolution as a low energy checkpoint, triggering multiple biological adaptations designed to preserve energy and adapt to metabolic stress before the cell reaches a state of bioenergetic catastrophe that triggers cell death.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Metabolic adaptation by the AMPK
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Despite the low overall percentage of pyruvate available for mitochondrial synthesis, the high rate of glycolytic flux provides sufficient amounts for biosynthesis.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > The mitochondrion-from engine to biosynthetic hub
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: The remaining pyruvate from aerobic glycolysis that is not converted to lactate (~10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.
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
“To meet this challenge, metabolic activities are reorganized in proliferating cells resulting in an anabolic shift in cellular metabolism.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Glycolysis-metabolic reprogramming fuels cell growth and proliferation
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“leading to the theory that oncogene and tumor suppressor networks influence the metabolic shift in cancer.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Without such a strategy, cells undergo apoptosis.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In particular, the c-Myc proto-oncogene is a potent regulator of multiple metabolic pathways essential for cancer growth (Dang et al. 2008).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Dang et al. 2008
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In the paper
“Metabolic flux analysis has revealed that glutamine is used by proliferating cells to generate a pool of a-ketoglutarate, which can be metabolized through the TCA cycle to regenerate the OAA consumed by biosynthesis (DeBerardinis et al. 2007).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > The mitochondrion-from engine to biosynthetic hub
What the sources say
- Not checked yetcites DeBerardinis 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. 16
- Probably not a substantial claim. 6
None of the sources cited for this claim have been checked yet.
In the paper
“Enhanced glucose uptake visualized by FDG-PET correlates with poor prognosis and higher metabolic potential in many tumor types (Gatenby and Gillies 2004;Kroemer and Pouyssegur 2008)”
What the sources say
- Not checked yetcites Gatenby and Gillies 2004
- Not checked yetcites Kroemer and Pouyssegur 2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, tumors face two distinct metabolic challenges: (1) how to modify their cellular metabolism to support enhanced cell growth and proliferation, and (2) how to engage strategies of metabolic adaptation to survive periods of metabolic stress and maintain viability as the cells accumulate.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“AMPK is responsive to changes in the cellular AMP:ATP ratio and is activated by stresses that stimulate ATP consumption or inhibit ATP production (Hardie 2003).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Metabolic adaptation by the AMPK
What the sources say
- Not checked yetcites Hardie 2003
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Oncogenic c-Myc promotes increased aerobic glycolysis through the constitutive elevation of LDH-A (Shim et al. 1997;Osthus et al. 2000), as well as expression of enzymes involved in nucleotide and amino acid metabolism (Gordan et al. 2007).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Shim et al. 1997
- Not checked yetcites Osthus et al. 2000
- Not checked yetcites Gordan et al. 2007
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This fundamental metabolic switch (''metabolic transformation'') may confer a selective growth advantage and/or resistance to apoptosis to allow cancer cells to maintain mitochondrial bioenergetics and integrity during cell growth and proliferation (DeBerardinis et al. 2008).”
What the sources say
- Not checked yetcites DeBerardinis et al. 2008
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In the paper
“Activity of the pathway is deregulated in cancer through a variety of mechanisms, including activating mutations in PI3K (Samuels et al. 2004(Samuels et al. , 2005;;Jia et al. 2008) or PTEN loss (Cairns et al. 1997).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Samuels et al. 2004
- Not checked yetcites Samuels et al. 2005
- Not checked yetcites Jia et al. 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Inhibition of ACL results in decreased glucose-dependent lipid synthesis and impaired cell proliferation (Hatzivassiliou et al. 2005).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > The mitochondrion-from engine to biosynthetic hub
What the sources say
- Not checked yetcites Hatzivassiliou et al. 2005
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Protein translation is essential for tumor growth, and deregulated translation itself can be tumorigenic (Mamane et al. 2004).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Mamane et al. 2004
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, Myc transformed cells are exquisitely sensitive to glutamine levels and rapidly deplete their TCA cycle intermediates when glutamine availability is reduced (Yuneva et al. 2007).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Yuneva et al. 2007
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“TORC1 activity is kept in check by the tumor suppressors TSC1/ TSC2 and LKB1, which function to block mTOR activation through inhibition of the small GTPase Rheb; mutation of these genes leads to elevated mTOR activity and the development of hamartomas (Inoki et al. 2003;Corradetti et al. 2004;Shaw et al. 2004a).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Tumor suppressors and oncogenes constitute metabolic signaling networks
What the sources say
- Not checked yetcites Inoki et al. 2003
- Not checked yetcites Corradetti et al. 2004
- Not checked yetcites Shaw et al. 2004a
plaindirect- 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
“Major physiological strategies of metabolic adaptation include cell cycle inhibition, inhibition of biosynthetic pathways (lipid, protein synthesis), increases in bioenergetic pathways (b-oxidation, glycolysis, and OXPHOS), and induction of autophagy.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“HIF1a blocks pyruvate entry into the mitochondrion by up-regulating the PDH antagonist PDK1.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“AMPK mediates metabolic adaptation through several pathways, including down-regulation of fatty acid synthesis through inhibition of ACC1, translation inhibition by blocking TORC1 activity, and activation of p53.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- 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
“Transcriptional regulation of DRAM by p53 induces autophagy, the products of which can also fuel OXPHOS.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Failure to manage or correct bioenergetic imbalance leads to cytochrome c release from mitochondria and induction of apoptosis.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
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In the paper
“Other modifiers of Beclin-1 activity such as UVRAG and Bif display tumor suppressor properties (C.Liang et al. 2007;Takahashi et al. 2007)”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Autophagy as a tumor suppressor mechanism
What the sources say
- Not checked yetcites C.Liang et al. 2007 source
- Not checked yetcites Takahashi et al. 2007
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“AMPK phosphorylates p53 at Ser-15, which stimulates both its transcriptional activity and initiates a metabolic cell cycle checkpoint (Jones et al. 2005).”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Metabolic adaptation by the AMPK
What the sources say
- Not checked yetcites Jones et al. 2005
plaindirect- 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
“Bioenergetic stress activates AMPK through an LKB-dependent manner.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Low HIF1a protein levels are maintained in cells under normoxia through the action of VHL-mediated proteosomal degradation.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rag GTPases regulate TORC1 activity and autophagy in response to amino acid deprivation.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
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. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, any subsequent inability to induce autophagy under conditions of nutrient or oxygen deprivation could render tumors more susceptible to apoptosis by metabolic stress.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Autophagy as a tumor suppressor mechanism
hedgedconditional- 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 may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“LKB or p53 deficiency, while permissive for unchecked cell growth, renders cells more susceptible to death by metabolic stress.”
§ Tumor suppressors and cell metabolism: a recipe for cancer growth > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper relies on this without support.
In proliferating cancer cells, the majority (>90%) of pyruvate generated from glucose is converted to lactate by LDH-A and secreted rather than oxidized to completion.
“In proliferating cancer cells, the majority of the pyruvate generated from glucose (>90%) is converted to lactate by lactate dehydrogenase (LDH-A), where it is readily secreted into the extracellular environment rather than oxidized to completion.”
The paper relies on this without support.
Metabolism of glucose through the oxidative or nonoxidative arms of the pentose phosphate pathway generates ribose-5-phosphate, a key intermediate in nucleotide biosynthesis.
“Metabolism of glucose through the oxidative or nonoxidative arms of the pentose phosphate pathway (PPP) generates ribose-5phosphate (Rib-5-P), a key intermediate in nucleotide biosynthesis.”
The paper relies on this without support.
The oxidative arm of the PPP can produce NADPH, which supplies a pool of reducing equivalents for both nucleotide and fatty acid biosynthesis.
“The oxidative arm of the PPP can also produce NADPH, which supplies a pool of reducing equivalents for both nucleotide and fatty acid biosynthesis.”
The paper relies on this without support.
Pyruvate can be imported into the mitochondria and converted into substrates for the production of additional amino acids or fatty acid synthesis, and used to maintain mitochondrial membrane potential.
“Finally, pyruvate can be imported into the mitochondria and converted into substrates for the production of additional amino acids or fatty acid synthesis, and used to maintain mitochondrial membrane potential.”
The paper relies on this without support.
The remaining pyruvate from aerobic glycolysis that is not converted to lactate (~10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.
“The remaining pyruvate from aerobic glycolysis that is not converted to lactate (;10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.”
The paper relies on this without support.
A solid tumor can outstrip its nutrient and oxygen supply as it grows, resulting in metabolic stress.
“A solid tumor can outstrip its nutrient and oxygen supply as it grows, resulting in metabolic stress (tumors experiencing metabolic stress are depicted in gray).”
The paper relies on this without support.
Tumor cells must undergo a period of metabolic adaptation to survive metabolic stress or undergo apoptosis.
“As a consequence, tumor cells must undergo a period of metabolic adaptation to survive this metabolic stress or undergo apoptosis.”
The paper relies on this without support.
PI3K is a central regulator of metabolism in both nontransformed and transformed cells.
“A central regulator of metabolism in both nontransformed and transformed cells is the phosphatidylinositol 3-kinase (PI3K), a lipid kinase that regulates the levels of phosphorylated phosphatidylinositol (PIP 3 ) at the plasma membrane.”
The paper relies on this without support.
Growth factor-dependent activation of PI3K leads to activation of downstream effectors including Akt and mTOR that coordinate metabolic activities supporting cellular biosynthesis.
“Growth factor-dependent activation of PI3K leads to the activation of downstream effectors including Akt and the mammalian target of rapamycin (mTOR) that coordinate metabolic activities that support cellular biosynthesis.”
The paper relies on this without support.
mTOR coordinates protein synthesis by regulating amino acid uptake, tRNA charging, and translation initiation.
“mTOR coordinates protein synthesis by regulating amino acid uptake, tRNA charging, and translation initiation.”
The paper relies on this without support.
Myc is a transcription factor activated by growth factor stimulation and is essential for the regulation of proliferation and cell cycle entry in nontransformed cells.
“Myc is a transcription factor activated by growth factor stimulation and is essential for the regulation of proliferation and cell cycle entry in nontransformed cells.”
The paper relies on this without support.
AMPK is activated under conditions of energetic stress, such as that triggered by nutrient deprivation or hypoxia.
“As a cellular sensor of AMP levels, AMPK is activated under conditions of energetic stress, such as that triggered by nutrient deprivation or hypoxia.”
The paper relies on this without support.
Beclin-1 is required for autophagy induction in mammalian cells.
“Studies involving Beclin-1, which is required for autophagy induction in mammalian cells, suggest that autophagy functions as an important tumor suppressor mechanism.”
The paper relies on this without support.
SDH and FH function as tumor suppressors in humans.
“However, the fact that metabolic enzymes such as SDH and FH function as tumor suppressors in humans suggests that metabolic deregulation can be an initiating event in cancer.”
The paper relies on this without support.
Cancer cells can become dependent on the activity of a specific oncogene for function and survival (oncogene addiction).
“In cancer cells, a given transformation event (i.e., oncogene activation) may play a qualitatively different or essential role in a given pathway compared with its role in normal cells, such that cancer cells become dependent on the activity of a specific oncogene for function and survival, a concept known as oncogene addiction.”
Claims other papers make about this one
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In the citing paper
“Tumor-promoting mutations in these genes tend to converge on a metabolic phenotype of enhanced glycolysis and energy production, thereby contributing to self-sufficiency of growth and evasion of growth-suppressive signals.”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Jones and Thompson, 2009
The cited source says what the claim attributes to it.
In the citing paper
“It is known that cancer cells preferentially use glycolysis instead of respiration to obtain energy (Warburg effect) (20).”
From Mitochondrial Dysfunction Contributes to Oncogene-Induced Senescence (2009) · cites this paper as [20]
In the citing paper
“Cellular transformation is a multistep process requiring acquisition of activated oncogenes and loss of tumor-suppressor genes, leading to usurpation of cellular signaling pathways controlling proliferation, survival, and metabolism 65, 66.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [66]
In the citing paper
“First, many human oncogenes and tumor suppressors regulate glucose metabolism (Figure 3A) (DeBerardinis, 2008; Jones and Thompson, 2009).”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Jones and Thompson, 2009
Citations
Cites
1 retracted
RETRACTED: Elevated tRNAiMet Synthesis Can Drive Cell Proliferation and Oncogenic Transformation
Marshall, L., Kenneth, N. S., & White, R. J. (2008) · Cell · doi:10.1016/j.cell.2008.02.035 · Cited by 134
RetractedWarburg, O. (1956) · Science · doi:10.1126/science.123.3191.309 · Cited by 13,425
p53, the cellular gatekeeper for growth and division
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Self-citationTargeting the hallmarks of cancer with therapy-induced endoplasmic reticulum (ER) stress
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Metadata
- Authors
- Jones, R. G., & Thompson, C. B.
- Affiliations
- McGill University (CA)
- Abramson Cancer Center (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2009-03-01
- Volume
- 23
- Issue
- 5
- Pages
- 537-548
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC2763495
- OpenAlex
- W2127049578
- Semantic Scholar
- f40e1cdc46be710b4cc935547b39b521d22208fa
- Cited by
- 1,085
- References
- 122
- Citations by year
- 2026: 11 · 2025: 39 · 2024: 30 · 2023: 54 · 2022: 50 · 2021: 63 · 2020: 56 · 2019: 66 · 2018: 69 · 2017: 68 · 2016: 69 · 2015: 78 · 2014: 100 · 2013: 97 · 2012: 87
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- McGill University
- National Institutes of Health
- Canadian Institutes of Health Research
- National Cancer Institute (R01CA105463)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- tumor suppressor, cancer metabolism, tumor growth, oncogenic mutations, metabolic regulation, cell proliferation, nutrient availability, oxygen availability, tumor vasculature, biosynthesis, bioenergetics
- MeSH terms
- Animals, Autophagy, Cells, Glycolysis, Humans, Mitochondria, Neoplasms, Oncogenes, Signal Transduction, Genes, Tumor Suppressor, Cell Proliferation, AMP-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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