Evidence map›Paper›PMID 36230918›Full record

ReviewCells2022

Therapeutic Drug-Induced Metabolic Reprogramming in Glioblastoma.

Trang T T Nguyen, Enyuan Shang, Mike-Andrew Westhoff, Georg Karpel-Massler, Markus D Siegelin

Abstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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.

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

16 citing papers in PubMed.

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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

5 authors.

Trang T T NguyenDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA.ORCID 0000-0001-8747-9082
Enyuan ShangDepartment of Biological Sciences, Bronx Community College, City University of New York, Bronx, NY 10453, USA.
Mike-Andrew WesthoffDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, 89075 Ulm, Germany.ORCID 0000-0003-3256-7100
Georg Karpel-MasslerDepartment of Neurosurgery, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0000-0001-8236-5369
Markus D SiegelinDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA.

Funding

HDAC Inhibitors Reverse the Warburg Effect and Elicit Metabolic Vulnerabilities in Model Systems of GlioblastomaR01NS113793 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SIEGELIN, MARKUS D · 2021 to 2025
$2.0M
Targeting Mutant IDH1 for a Novel Synthetic Lethal Interaction in Malignant GliomasR01NS102366 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SIEGELIN, MARKUS D · 2018 to 2022
$1.8M
Dual Inhibition of Mitochondrial Matrix Chaperones and Anti-Apoptotic Bcl-2 Family Members for Glioblastoma Therapy.R01NS095848 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SIEGELIN, MARKUS D · 2016 to 2020
$1.8M
NINDS NIH HHS R01 NS095848NINDS NIH HHS R01 NS102366NINDS NIH HHS R01 NS113793
6 · The paper itself

Abstract

Glioblastoma WHO IV (GBM), the most common primary brain tumor in adults, is a heterogenous malignancy that displays a reprogrammed metabolism with various fuel sources at its disposal. Tumor cells primarily appear to consume glucose to entertain their anabolic and catabolic metabolism. While less effective for energy production, aerobic glycolysis (Warburg effect) is an effective means to drive biosynthesis of critical molecules required for relentless growth and resistance to cell death. Targeting the Warburg effect may be an effective venue for cancer treatment. However, past and recent evidence highlight that this approach may be limited in scope because GBM cells possess metabolic plasticity that allows them to harness other substrates, which include but are not limited to, fatty acids, amino acids, lactate, and acetate. Here, we review recent key findings in the literature that highlight that GBM cells substantially reprogram their metabolism upon therapy. These studies suggest that blocking glycolysis will yield a concomitant reactivation of oxidative energy pathways and most dominantly beta-oxidation of fatty acids.

Indexed as

GlioblastomaAmino AcidsFatty AcidsGlucoseHumansLactic AcidOxidative PhosphorylationAmino AcidsFatty AcidsGlucoseLactic Acidglioblastomaglycolysismetabolismoxidative phosphorylation (OXPHOS)TCA cycle

Identifiers

PMID36230918
PMCPMC9563867

What OpenQuestion holds

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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.