Evidence map›Paper›PMID 28212543›Full record

ReviewOncotarget2017

Metabotropic glutamate receptors as a new therapeutic target for malignant gliomas.

Mery Stefani Leivas Pereira, Fábio Klamt, Chairini Cássia Thomé, Paulo Valdeci Worm, Diogo Losch de Oliveira

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Role of nerves in neurofibromatosis type 1-related nervous system tumors.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Glutamate in cancers: from metabolism to signaling.Journal of biomedical research · 2019
    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

5 authors at 2 institutions in 1 country.

Mery Stefani Leivas PereiraDepartment of Biochemistry, Laboratory of Cellular Neurochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil.
Fábio KlamtDepartment of Biochemistry, Laboratory of Cellular Biochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil.
Chairini Cássia ThoméDepartment of Biochemistry, Laboratory of Cellular Neurochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil.
Paulo Valdeci WormDepartment of Neurosurgery, Cristo Redentor Hospital - GHC - Porto Alegre RS, Brazil.
Diogo Losch de OliveiraDepartment of Biochemistry, Laboratory of Cellular Neurochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil.
Universidade Federal do Rio Grande do Sul · BRFaculdade Redentor · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabotropic glutamate receptors (mGluR) are predominantly involved in maintenance of cellular homeostasis of central nervous system. However, evidences have suggested other roles of mGluR in human tumors. Aberrant mGluR signaling has been shown to participate in transformation and maintenance of various cancer types, including malignant brain tumors. This review intends to summarize recent findings regarding the involvement of mGluR-mediated intracellular signaling pathways in progression, aggressiveness, and recurrence of malignant gliomas, mainly glioblastomas (GBM), highlighting the potential therapeutic applications of mGluR ligands. In addition to the growing number of studies reporting mGluR gene or protein expression in glioma samples (resections, lineages, and primary cultures), pharmacological blockade in vitro of mGluR1 and mGluR3 by selective ligands has been shown to be anti-proliferative and anti-migratory, decreasing activation of MAPK and PI3K pathways. In addition, mGluR3 antagonists promoted astroglial differentiation of GBM cells and also enabled cytotoxic action of temozolomide (TMZ). mGluR3-dependent TMZ toxicity was supported by increasing levels of MGMT transcripts through an intracellular signaling pathway that sequentially involves PI3K and NF-κB. Further, continuous pharmacological blockade of mGluR1 and mGluR3 have been shown to reduced growth of GBM tumor in two independent in vivo xenograft models. In parallel, low levels of mGluR3 mRNA in GBM resections may be a predictor for long survival rate of patients. Since several Phase I, II and III clinical trials are being performed using group I and II mGluR modulators, there is a strong scientifically-based rationale for testing mGluR antagonists as an adjuvant therapy for malignant brain tumors.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsGliomaHumansReceptors, Metabotropic GlutamateAntineoplastic AgentsReceptors, Metabotropic Glutamatebrain cancerglioblastomamGluR

Identifiers

PMID28212543
PMCPMC5400663
OpenAlexW2588760673

What OpenQuestion holds

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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.