Evidence map›Paper›PMID 33673213›Full record

ReviewInternational journal of molecular sciences2021

Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.

Manali Tilak, Jennifer Holborn, Laura A New, Jasmin Lalonde, Nina Jones

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
7.4field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Systemic Drug Effects in Vortioxetine-Induced Time-Series Datasets.International journal of molecular sciences · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Association of tumor treating fields (TTFields) therapy with overall survival in newly diagnosed glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  13. Article
  14. Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases.International journal of molecular sciences · 2025
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Manali TilakDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, ON N1G 2W1, Canada.
Jennifer HolbornDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, ON N1G 2W1, Canada.ORCID 0000-0001-7370-8016
Laura A NewDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, ON N1G 2W1, Canada.
Jasmin LalondeDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, ON N1G 2W1, Canada.ORCID 0000-0002-6797-1894
Nina JonesDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, ON N1G 2W1, Canada.ORCID 0000-0003-2786-2404
University of Guelph · CA

Funding

Natural Sciences and Engineering Research Council of Canada RGPIN 461433-2017
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is amongst the deadliest of human cancers, with a median survival rate of just over one year following diagnosis. Characterized by rapid proliferation and diffuse infiltration into the brain, GBM is notoriously difficult to treat, with tumor cells showing limited response to existing therapies and eventually developing resistance to these interventions. As such, there is intense interest in better understanding the molecular alterations in GBM to guide the development of more efficient targeted therapies. GBM tumors can be classified into several molecular subtypes which have distinct genetic signatures, and they show aberrant activation of numerous signal transduction pathways, particularly those connected to receptor tyrosine kinases (RTKs) which control glioma cell growth, survival, migration, invasion, and angiogenesis. There are also non-canonical modes of RTK signaling found in GBM, which involve G-protein-coupled receptors and calcium channels. This review uses The Cancer Genome Atlas (TCGA) GBM dataset in combination with a data-mining approach to summarize disease characteristics, with a focus on select molecular pathways that drive GBM pathogenesis. We also present a unique genomic survey of RTKs that are frequently altered in GBM subtypes, as well as catalog the GBM disease association scores for all RTKs. Lastly, we discuss current RTK targeted therapies and highlight emerging directions in GBM research.

Indexed as

Cell ProliferationSignal TransductionBrain NeoplasmsGlioblastomaHumansNeoplasm ProteinsPhosphorylationReceptor Protein-Tyrosine KinasesNeoplasm ProteinsReceptor Protein-Tyrosine Kinasescalciumglioblastoma multiformereceptor tyrosine kinasetyrosine kinase inhibitors

Identifiers

PMID33673213
PMCPMC7918566
OpenAlexW3130202064

What Socratic 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 Socratic graph.