Evidence map›Paper›PMID 30511933›Full record

ArticleRadiology and oncology2018

Nuclear magnetic resonance metabolic fingerprint of bevacizumab in mutant IDH1 glioma cells.

Tanja Mesti, Nadia Bouchemal, Claire Banissi, Mohamed N Triba, Carole Marbeuf-Gueye, Maja Cemazar, Laurence Le Moyec, Antoine F Carpentier, Philippe Savarin, Janja Ocvirk

Open access · goldAbstract read
In one paragraph

Article in Radiology and oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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

10 authors at 5 institutions in 2 countries.

Tanja MestiLaboratoire de Recherches Biochirurgicales, Université Paris Descartes, Hôpital Européen Georges Pompidou, paris, France.
Nadia BouchemalCSPBAT, UMR 7244, CNRS, Université Paris 13, Sorbonne Paris Cité, Bobigny, France.
Claire BanissiLaboratoire de Recherches Biochirurgicales, Université Paris Descartes, Hôpital Européen Georges Pompidou, paris, France.
Mohamed N TribaCSPBAT, UMR 7244, CNRS, Université Paris 13, Sorbonne Paris Cité, Bobigny, France.
Carole Marbeuf-GueyeCSPBAT, UMR 7244, CNRS, Université Paris 13, Sorbonne Paris Cité, Bobigny, France.
Maja CemazarDepartment of Experimental Oncology, Institute of Oncology Ljubljana, Ljubljana, Slovenia.
Laurence Le MoyecUnité de Biologie Intégrative des Adaptations à l'Exercice, Université d'Evry, Evry, France.
Antoine F CarpentierLaboratoire de Recherches Biochirurgicales, Université Paris Descartes, Hôpital Européen Georges Pompidou, paris, France.
Philippe SavarinDepartment of Experimental Oncology, Institute of Oncology Ljubljana, Ljubljana, Slovenia.
Janja OcvirkDivision of Medical Oncology, Institute of Oncology Ljubljana, Ljubljana, Slovenia.
Institute of Oncology Ljubljana · SIChimie, Structures et Propriétés de Biomatériaux et d'Agents ThérapeutiquesDélégation Paris 5 · FRHôpital Européen Georges-Pompidou · FRSorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Malignant gliomas are rapidly growing tumours that extensively invade the brain and have bad prognosis. Our study was performed to assess the metabolic effects of bevacizumab on the glioma cells carrying the IDH1 mutation, a mutation, associated with better prognosis and treatment outcome. Bevacizumab is known to inhibit tumour growth by neutralizing the biological activity of vascular endothelial growth factor (VEGF). However, the direct effects of bevacizumab on tumour cells metabolism remain poorly known. Materials and methods The immunoassay and MTT assay were used to assess the concentration of secreted VEGF and cell viability after bevacizumab exposure. Metabolomic studies on cells were performed using high resolution magic angle spinning spectroscopy (HRMAS). Results mIDH1-U87 cells secreted VEGF (13 ng/mL). Regardless, bevacizumab had no cytotoxic effect, even after a 72h exposure and with doses as high as 1 mg/mL. Yet, HRMAS analysis showed a significant effect of bevacizumab (0.1 mg/mL) on the metabolic phenotype of mIDH1-U87 cells with elevation of 2-hydroxyglutarate and changes in glutamine group metabolites (alanine, glutamate, glycine) and lipids (polyunsaturated fatty acids [PUFA], glycerophosphocholine, and phosphocholine). Conclusions In mIDH1-U87 cells, changes in glutamine group metabolites and lipids were identified as metabolic markers of bevacizumab treatment. These data support the possibility of a functional tricarboxylic acid cycle that runs in reductive manner, as a probable mechanism of action of bevacizumab in IDH1 mutated gliomas and propose a new target pathway for effective treatment of malignant gliomas.

Indexed as

Angiogenesis InhibitorsAntibodies, Monoclonal, HumanizedApoptosisBevacizumabBiomarkers, TumorBrain NeoplasmsCell Line, TumorCell SurvivalEnzyme-Linked Immunosorbent AssayGliomaHumansMagnetic Resonance SpectroscopyPhenotypePrincipal Component AnalysisVascular Endothelial Growth Factor AAngiogenesis InhibitorsAntibodies, Monoclonal, HumanizedBevacizumabBiomarkers, TumorVascular Endothelial Growth Factor Abevacizumabfingerprintidh1 mutationmalignant gliomametabolic

Identifiers

PMID30511933
PMCPMC6287186
OpenAlexW2902083973

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.