Evidence map›Paper›PMID 28629170›Full record

ReviewInternational journal of molecular sciences2017

EGFR and EGFRvIII Promote Angiogenesis and Cell Invasion in Glioblastoma: Combination Therapies for an Effective Treatment.

Stefanie Keller, Mirko H H Schmidt

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. Review
  3. Immunohistochemical evaluation of EGFR protein expression and microvascular density reveals an angiogenic signature in Tunisian patients with metastatic colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  4. Review
  5. Article
  6. Structure-Activity Relationships ofPharmaceuticals (Basel, Switzerland) · 2025
    Article
  7. Article
  8. Article
  9. Review
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  11. Article
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  13. Review
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  16. Review
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  18. Article
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Stefanie KellerMolecular Signal Transduction Laboratories, Institute for Microscopic Anatomy and Neurobiology, Focus Program Translational Neuroscience (FTN), Rhine Mainz Neuroscience Network (rmn2), Johannes Gutenberg University, School of Medicine, 55131 Mainz, Germany. stefanie.keller@unimedizin-mainz.de.
Mirko H H SchmidtMolecular Signal Transduction Laboratories, Institute for Microscopic Anatomy and Neurobiology, Focus Program Translational Neuroscience (FTN), Rhine Mainz Neuroscience Network (rmn2), Johannes Gutenberg University, School of Medicine, 55131 Mainz, Germany. mirko.schmidt@unimedizin-mainz.de.
German Cancer Research Center · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) and the mutant EGFRvIII are major focal points in current concepts of targeted cancer therapy for glioblastoma multiforme (GBM), the most malignant primary brain tumor. The receptors participate in the key processes of tumor cell invasion and tumor-related angiogenesis and their upregulation correlates with the poor prognosis of glioma patients. Glioma cell invasion and increased angiogenesis share mechanisms of the degradation of the extracellular matrix (ECM) through upregulation of ECM-degrading proteases as well as the activation of aberrant signaling pathways. This review describes the role of EGFR and EGFRvIII in those mechanisms which might offer new combined therapeutic approaches targeting EGFR or EGFRvIII together with drug treatments against proteases of the ECM or downstream signaling to increase the inhibitory effects of mono-therapies.

Indexed as

AnimalsBrain NeoplasmsCombined Modality TherapyErbB ReceptorsGlioblastomaHumansMolecular Targeted TherapyNeovascularization, Pathologicepidermal growth factor receptor VIIIErbB ReceptorsangiogenesisEGFREGFRvIIIglioblastoma multiformeinvasion

Identifiers

PMID28629170
PMCPMC5486116
OpenAlexW2625826824

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.