Evidence map›Paper›PMID 31025151›Full record

ArticleNeurochemical research2019

Provocative Question: Should Ketogenic Metabolic Therapy Become the Standard of Care for Glioblastoma?

Thomas N Seyfried, Laura Shelton, Gabriel Arismendi-Morillo, Miriam Kalamian, Ahmed Elsakka, Joseph Maroon, Purna Mukherjee

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  9. Pharmacological inhibition of ENT1 enhances the impact of specific dietary fats on energy metabolism gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 4 institutions in 3 countries.

Thomas N SeyfriedBiology Department, Boston College, 140 Commonwealth Ave, Chestnut Hill, MA, 02467, USA. Thomas.seyfried@bc.edu.
Laura SheltonHuman Metabolome Technologies America, 24 Denby Rd., Boston, MA, 02134, USA.
Gabriel Arismendi-MorilloInstituto de Investigaciones Biológicas, Facultad de Medicina, Universidad del Zulia, Maracaibo, 526, Venezuela.
Miriam KalamianDietary Therapies Llc., Hamilton, MT, USA.
Ahmed ElsakkaFaculty of Medicine, University of Alexandria, Alexandria, Egypt.
Joseph MaroonDepartment of Neurosurgery, University of Pittsburgh Medical Center, Suite 5C, 200 Lothrop St., Pittsburgh, PA, USA.
Purna MukherjeeBiology Department, Boston College, 140 Commonwealth Ave, Chestnut Hill, MA, 02467, USA.
Boston College · USAlexandria University · EGUniversity of Pittsburgh Medical Center · USUniversity of Zulia · VE

Funding

Glycosphingolipid Effects on Brain Tumor AngiogenesisR01CA102135 · NCI · BOSTON COLLEGE · PI SEYFRIED, THOMAS N · 2004 to 2006
$734k
CrossFit 51o5681Foundation for Metabolic Cancer Therapies 5101551NCI NIH HHS R01 CA102135Nelson Mandela Metropolitan University (ZA) 116600
6 · The paper itself

Abstract

No major advances have been made in improving overall survival for glioblastoma (GBM) in almost 100 years. The current standard of care (SOC) for GBM involves immediate surgical resection followed by radiotherapy with concomitant temozolomide chemotherapy. Corticosteroid (dexamethasone) is often prescribed to GBM patients to reduce tumor edema and inflammation. The SOC disrupts the glutamate-glutamine cycle thus increasing availability of glucose and glutamine in the tumor microenvironment. Glucose and glutamine are the prime fermentable fuels that underlie therapy resistance and drive GBM growth through substrate level phosphorylation in the cytoplasm and the mitochondria, respectively. Emerging evidence indicates that ketogenic metabolic therapy (KMT) can reduce glucose availability while elevating ketone bodies that are neuroprotective and non-fermentable. Information is presented from preclinical and case report studies showing how KMT could target tumor cells without causing neurochemical damage thus improving progression free and overall survival for patients with GBM.

Indexed as

Standard of CareBrain NeoplasmsGlioblastomaGlucoseGlutamineHumansKetone BodiesMitochondriaTemozolomideTumor MicroenvironmentGlucoseGlutamineKetone BodiesTemozolomideFermentationGlucoseGlutamateGlutamineKetogenic dietSubstrate level phosphorylationWarburg

Identifiers

PMID31025151
OpenAlexW2941260093

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.