Evidence map›Paper›PMID 25113866›Full record

ArticleNeuromolecular medicine2014

Direct effect of bevacizumab on glioblastoma cell lines in vitro.

Thomas Simon, Bérénice Coquerel, Alexandre Petit, Yusra Kassim, Elise Demange, Didier Le Cerf, Valérie Perrot, Jean-Pierre Vannier

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. From Donor to the Lab: A Fascinating Journey of Primary Cell Lines.Frontiers in cell and developmental biology · 2021
    Review
  13. Review
  14. Article
  15. Integration of CaOncogene · 2018
    Article
  16. Article
  17. Macropinocytosis of Bevacizumab by Glioblastoma Cells in the Perivascular Niche Affects their Survival.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  18. Review
  19. Article
  20. Review
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

8 authors.

Thomas SimonGroupe de Recherche «Micro-Environnement et Renouvellement Cellulaire Intégrés» MERCI UPRES EA 3829, Faculté de Médecine et Pharmacie, Université de Rouen, 22 Boulevard Gambetta, 76183, Rouen Cedex, France, thomas.simon1@univ-rouen.fr.
Bérénice Coquerel
Alexandre Petit
Yusra Kassim
Elise Demange
Didier Le Cerf
Valérie Perrot
Jean-Pierre Vannier

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bevacizumab is a humanized monoclonal antibody directed against the pro-angiogenic factor vascular and endothelial growth factor-A (VEGF-A) used in the treatment of glioblastomas. Although most patients respond initially to this treatment, studies have shown that glioblastomas eventually recur. Several non-mutually exclusive theories based on the anti-angiogenic effect of bevacizumab have been proposed to explain these mechanisms of resistance. In this report, we studied whether bevacizumab can act directly on malignant glioblastoma cells. We observe changes in the expression profiles of components of the VEGF/VEGF-R pathway and in the response to a VEGF-A stimulus following bevacizumab treatment. In addition, we show that bevacizumab itself acts on glioblastoma cells by activating the Akt and Erks survival signaling pathways. Bevacizumab also enhances proliferation and invasiveness of glioblastoma cells in hyaluronic acid hydrogel. We propose that the paradoxical effect of bevacizumab on glioblastoma cells could be due to changes in the VEGF-A-dependent autocrine loop as well as in the intracellular survival pathways, leading to the enhancement of tumor aggressiveness. Investigation of how bevacizumab interacts with glioblastoma cells and the resulting downstream signaling pathways will help targeting populations of resistant glioblastoma cells.

Indexed as

Angiogenesis InhibitorsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsAutocrine CommunicationBevacizumabBrain NeoplasmsCalcium SignalingCell Culture TechniquesCell DivisionCell Line, TumorCell MovementDrug Resistance, NeoplasmDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticGlioblastomaHumansAKT1 protein, humanAngiogenesis InhibitorsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBevacizumabHyaluronic AcidHydrogelsIndolesKDR protein, humanNeoplasm ProteinsPGF protein, humanPlacenta Growth FactorPregnancy ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPyrrolesSunitinibVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2VEGFA protein, human

Identifiers

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.