Evidence map›Paper›PMID 20824044›Full record

ReviewNeoplasia (New York, N.Y.)2010

Epidermal growth factor receptor in glioma: signal transduction, neuropathology, imaging, and radioresistance.

Kimmo J Hatanpaa, Sandeep Burma, Dawen Zhao, Amyn A Habib

Open access · goldAbstract readReview
In one paragraph

Review in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed, 5 pooled it
13.6field-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

236 citing papers in PubMed, 5 syntheses or guidelines pooled it, 467 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Molecular Biomarkers in Glioblastoma: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022
    Pooled it
  5. Pooled it
  6. Article
  7. Article
  8. Review
  9. Sialylation Inhibition Impairs Migration and Promotes Adhesion of GBM Cells.International journal of molecular sciences · 2025
    Article
  10. Article
  11. Article
  12. Nano-Based Technology in Glioblastoma.Molecules (Basel, Switzerland) · 2025
    Review
  13. Review
  14. Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025
    Review
  15. Review
  16. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Review

176 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

4 authors at 1 institution in 1 country.

Kimmo J HatanpaaDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Sandeep Burma
Dawen Zhao
Amyn A Habib
The University of Texas Southwestern Medical Center · US

Funding

A Role for RIP1 in GliomagenesisR01NS062080 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HABIB, AMYN · 2009 to 2012
$1.2M
Dynamic multimodal imaging of tumor hypoxia and vascular profiles in glioblastomaR21CA141348 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHAO, DAWEN · 2010 to 2011
$340k
NCI NIH HHS 1R21 CA141348-01A1NCI NIH HHS R21 CA141348NINDS NIH HHS R01 NS062080NINDS NIH HHS R01NS062080-01A2
6 · The paper itself

Abstract

Aberrant epidermal growth factor receptor (EGFR) signaling is common in cancer. Increased expression of wild type and mutant EGFR is a widespread feature of diverse types of cancer. EGFR signaling in cancer has been the focus of intense investigation for decades primarily for two reasons. First, aberrant EGFR signaling is likely to play an important role in the pathogenesis of cancer, and therefore, the mechanisms of EGFR-mediated oncogenic signaling are of interest. Second, the EGFR signaling system is an attractive target for therapeutic intervention. EGFR gene amplification and overexpression are a particularly striking feature of glioblastoma (GBM), observed in approximately 40% of tumors. GBM is the most common primary malignant tumor of the central nervous system in adults. In approximately 50% of tumors with EGFR amplification, a specific EGFR mutant (EGFRvIII, also known as EGFR type III, de2-7, Delta EGFR) can be detected. This mutant is highly oncogenic and is generated from a deletion of exons 2 to 7 of the EGFR gene, which results in an in-frame deletion of 267 amino acids from the extracellular domain of the receptor. EGFRvIII is unable to bind ligand, and it signals constitutively. Although EGFRvIII has the same signaling domain as the wild type receptor, it seems to generate a distinct set of downstream signals that may contribute to an increased tumorigenicity. In this review, we discuss recent progress in key aspects of EGFR signaling in GBM, focusing on neuropathology, signal transduction, imaging of the EGFR, and the role of the EGFR in mediating resistance to radiation therapy in GBM.

Indexed as

Brain NeoplasmsGliomaAdultDiagnostic ImagingErbB ReceptorsHumansModels, BiologicalMolecular Targeted TherapyMutant ProteinsRadiation ToleranceRadiopharmaceuticalsSignal TransductionErbB ReceptorsMutant ProteinsRadiopharmaceuticals

Identifiers

PMID20824044
PMCPMC2933688
OpenAlexW2103744931

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.