Evidence map›Paper›PMID 36338708›Full record

ArticleFrontiers in oncology2022

GBM tumors are heterogeneous in their fatty acid metabolism and modulating fatty acid metabolism sensitizes cancer cells derived from recurring GBM tumors to temozolomide.

Sweta Parik, Juan Fernández-García, Francesca Lodi, Karen De Vlaminck, Marleen Derweduwe, Steven De Vleeschouwer, Raf Sciot, Wietse Geens, Linqian Weng, Francesca Maria Bosisio and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

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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

16 authors at 5 institutions in 2 countries.

Sweta ParikLaboratory of Cellular Metabolism and Metabolic Regulation, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Juan Fernández-GarcíaLaboratory of Cellular Metabolism and Metabolic Regulation, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Francesca LodiLaboratory for Translational Genetics, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Karen De VlaminckLaboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Marleen DerweduweLaboratory for Precision Cancer Medicine, Translational Cell and Tissue Research, Department of Imaging & Pathology, KU Leuven, Leuven, Belgium.
Steven De VleeschouwerDepartment of Neurosurgery, University Hospital Leuven, Leuven, Belgium.
Raf SciotDepartment of Pathology, University Hospital Leuven, KU Leuven, Leuven, Belgium.
Wietse GeensDepartment of Neurosurgery, UZ Brussel, Jette, Belgium.
Linqian WengLaboratory of Tumor Microenvironment and Therapeutic Resistance, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Francesca Maria BosisioDepartment of Pathology, University Hospital Leuven, KU Leuven, Leuven, Belgium.
Gabriele BergersLaboratory of Tumor Microenvironment and Therapeutic Resistance, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Johnny DuerinckDepartment of Neurosurgery, UZ Brussel, Jette, Belgium.
Frederick De SmetLaboratory for Precision Cancer Medicine, Translational Cell and Tissue Research, Department of Imaging & Pathology, KU Leuven, Leuven, Belgium.
Diether LambrechtsLaboratory for Translational Genetics, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Jo A Van GinderachterLaboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Sarah-Maria FendtLaboratory of Cellular Metabolism and Metabolic Regulation, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
KU Leuven · BEVIB-KU Leuven Center for Cancer Biology · BEUniversitair Ziekenhuis Brussel · BEVrije Universiteit Brussel · BEVIB-UGent Center for Inflammation Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is a highly lethal grade of astrocytoma with very low median survival. Despite extensive efforts, there is still a lack of alternatives that might improve these prospects. We uncovered that the chemotherapeutic agent temozolomide impinges on fatty acid synthesis and desaturation in newly diagnosed glioblastoma. This response is, however, blunted in recurring glioblastoma from the same patient. Further, we describe that disrupting cellular fatty acid homeostasis in favor of accumulation of saturated fatty acids such as palmitate synergizes with temozolomide treatment. Pharmacological inhibition of SCD and/or FADS2 allows palmitate accumulation and thus greatly augments temozolomide efficacy. This effect was independent of common GBM prognostic factors and was effective against cancer cells from recurring glioblastoma. In summary, we provide evidence that intracellular accumulation of saturated fatty acids in conjunction with temozolomide based chemotherapy induces death in glioblastoma cells derived from patients.

Indexed as

FADS2fatty acid metabolismglioblastomalipotoxicitySCD1tumor heterogeneity

Identifiers

PMID36338708
PMCPMC9635944
OpenAlexW4296823039

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.