Evidence map›Paper›PMID 24343361›Full record

ReviewCarcinogenesis2014

Cancer as a metabolic disease: implications for novel therapeutics.

Thomas N Seyfried, Roberto E Flores, Angela M Poff, Dominic P D'Agostino

2 registry-linked trialsAbstract readReview
In one paragraph

Review in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 260 papers.

0numbers the graph read from it
0cells of the map it votes in
260citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03221920 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Effect of Very Low Carbohydrate Diet to Glasgow Prognostic Score, Serum Lactate and TNF Alpha on Colorectal Cancer Patients With Best Supportive Care

TypeinterventionalSponsorDr. Soetomo General HospitalRan2017 to 2017Enrolled26ConditionsDiet Modification, Colorectal Adenocarcinoma, Systemic Inflammation, TNF AlphaArmsVery Low Carbohydrate Diet
NCT06987708 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

Evaluating the Impact of a 12-month Multi-Modal Lifestyle Management Intervention on Disease Relevant Biomarkers Associated With Monoclonal Gammopathy of Unknown Significance (MGUS) and Smoldering Myeloma (SM): A Prospective Intervention Pilot Study

TypeinterventionalSponsorHackensack Meridian HealthRan2026 to 2028Enrolled67ConditionsMonoclonal Gammopathy of Uncertain Significance, Smoldering MyelomaArmsThe Multimodal Lifestyle Intervention
3 · Its place in the literature

Who cites it

260 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. The biological functions of monoacylglycerol lipase (MAGL) in cancer.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

200 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Thomas N SeyfriedBiology Department, Boston College, Chestnut Hill, MA 02467, USA and.
Roberto E Flores
Angela M Poff
Dominic P D'Agostino

Funding

Glycosphingolipids in murine neurodegenerative diseasesR01NS055195 · NINDS · BOSTON COLLEGE · PI SEYFRIED, THOMAS N · 2006 to 2009
$1.5M
GLYCOSPHINGOLIPIDS IN MURINE NEURODEGENERATIVE DISEASESR01HD039722 · NICHD · BOSTON COLLEGE · PI SEYFRIED, THOMAS N · 2001 to 2004
$852k
Glycosphingolipid Effects on Brain Tumor AngiogenesisR01CA102135 · NCI · BOSTON COLLEGE · PI SEYFRIED, THOMAS N · 2004 to 2006
$734k
Glycosphingolipids in Murine Neurodegenerative DiseasesR56NS055195 · NINDS · BOSTON COLLEGE · PI SEYFRIED, THOMAS N · 2012 to 2012
$346k
NCI NIH HHS CA-102135NICHD NIH HHS HD-39722NINDS NIH HHS NS-55195
6 · The paper itself

Abstract

Emerging evidence indicates that cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation. The genomic instability observed in tumor cells and all other recognized hallmarks of cancer are considered downstream epiphenomena of the initial disturbance of cellular energy metabolism. The disturbances in tumor cell energy metabolism can be linked to abnormalities in the structure and function of the mitochondria. When viewed as a mitochondrial metabolic disease, the evolutionary theory of Lamarck can better explain cancer progression than can the evolutionary theory of Darwin. Cancer growth and progression can be managed following a whole body transition from fermentable metabolites, primarily glucose and glutamine, to respiratory metabolites, primarily ketone bodies. As each individual is a unique metabolic entity, personalization of metabolic therapy as a broad-based cancer treatment strategy will require fine-tuning to match the therapy to an individual's unique physiology.

Indexed as

Energy MetabolismGenes, p53Genes, rasHumansMitochondriaMutationNeoplasms

Identifiers

PMID24343361
PMCPMC3941741

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.