Evidence map›Paper›PMID 26755074›Full record

ReviewNeuro-oncology2016

Epidermal growth factor receptor targeting and challenges in glioblastoma.

Amy Haseley Thorne, Ciro Zanca, Frank Furnari

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
11.7field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  5. Review
  6. Review
  7. Article
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  11. Article
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  14. Article
  15. Review
  16. The Role of Hyperexcitability in Gliomagenesis.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Review

23 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

3 authors at 2 institutions in 1 country.

Amy Haseley ThorneLudwig Institute for Cancer Research, University of California at San Diego, La Jolla, California (A.H.T., C.Z., F.F.); Moores Cancer Center, University of California at San Diego, La Jolla, California (F.F.); Department of Pathology, University of California at San Diego, La Jolla, California (F.F.).
Ciro ZancaLudwig Institute for Cancer Research, University of California at San Diego, La Jolla, California (A.H.T., C.Z., F.F.); Moores Cancer Center, University of California at San Diego, La Jolla, California (F.F.); Department of Pathology, University of California at San Diego, La Jolla, California (F.F.).
Frank FurnariLudwig Institute for Cancer Research, University of California at San Diego, La Jolla, California (A.H.T., C.Z., F.F.); Moores Cancer Center, University of California at San Diego, La Jolla, California (F.F.); Department of Pathology, University of California at San Diego, La Jolla, California (F.F.).
University of California, San Diego · USLudwig Cancer Research · US

Funding

Contemporary Approaches to Cancer Cell Signaling and CommunicationT32CA009523 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DONOGHUE, DANIEL J, YANG, JING · 1985 to 2025
$12.1M
Genotypic Interactions in Brain Cancer HeterogeneityR01NS080939 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FURNARI, FRANK · 2012 to 2022
$3.5M
NCI NIH HHS T32 CA009523NINDS NIH HHS R01 NS080939
6 · The paper itself

Abstract

With the evolution of technology, there is now a deeper understanding of glioblastoma as an inter- and intraheterogeneous disease comprising a multitude of genetically and epigenetically different cancer cells. Greater characterization of glioblastoma at the molecular level has improved its initial pathophysiological staging and classification. With this knowledge comes the hope that more efficacious therapies to combat this highly lethal disease are on the horizon. One possibility for intervention is represented by the targeting of epidermal growth factor receptor (EGFR), which is amplified and mutated in a large subset of patients. In this review, we provide a brief overview of EGFR and its mutated form, EGFR variant III, describing the downstream cellular pathways activated by each receptor, available animal models, therapeutic strategies to inhibit the receptor, and possible intervention routes to efficiently target this receptor and prevent the emergence of resistant mechanisms which to date have hampered a successful therapeutic outcome.

Indexed as

AnimalsBrain NeoplasmsDrug Resistance, NeoplasmErbB ReceptorsGlioblastomaHumansSignal TransductionEGFR protein, humanErbB ReceptorsEGFREGFRvIIIglioblastomagliomatherapy

Identifiers

PMID26755074
PMCPMC4896544
OpenAlexW2312738416

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.