Evidence map›Paper›PMID 12944901›Full record

ArticleOncogene2003

EGFRvIII-mediated radioresistance through a strong cytoprotective response.

Guido Lammering, Theodore H Hewit, Kristoffer Valerie, Joseph N Contessa, George P Amorino, Paul Dent, Rupert K Schmidt-Ullrich

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Targeting drug resistance in glioblastoma (Review).International journal of oncology · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Targeted therapy combined with radiotherapy in non-small-cell lung cancer: a review of the Oncologic Group for the Study of Lung Cancer (Spanish Radiation Oncology Society).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Current concepts in clinical radiation oncology.Radiation and environmental biophysics · 2014
    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

7 authors at 2 institutions in 2 countries.

Guido LammeringDepartment of Radiation Oncology, Heinrich-Heine University, Duesseldorf, Germany.
Theodore H Hewit
Kristoffer Valerie
Joseph N Contessa
George P Amorino
Paul Dent
Rupert K Schmidt-Ullrich
Virginia Commonwealth University Medical Center · USHeinrich Heine University Düsseldorf · DE

Funding

RADIOSENSITIZATION OF MALIGNANT GLIOMAS BY VIRAL TRANSDUCTION WITH WILD-TYPE P53P01CA072955 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI VALERIE, KRISTOFFER CARL · 1998 to 2007
$6.0M
RADIATION, ERBB ACTIVATION AND CELLULAR GROWTH CONTROLR01CA065896 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MIKKELSEN, ROSS B · 1995 to 2008
$2.0M
NCI NIH HHS P01 CA72955NCI NIH HHS R01 CA65896
6 · The paper itself

Abstract

The constitutively active, truncated epidermal growth factor receptor EGFRvIII lacks the ability of EGF binding due to a deletion of the NH(2)-terminal domain. EGFRvIII confers increased tumorigenicity, is coexpressed with EGFR wild type (wt) in human carcinoma and malignant glioma cells when grown as xenografts, but is not expressed in vitro. The effects of EGFRvIII expression on cellular radiation responses were studied in Chinese hamster ovary (CHO) cells transfected with plasmids expressing EGFRvIII (CHO.EGFRvIII) or EGFRwt (CHO.EGFRwt). CHO cells expressing similar levels of either receptor were employed to define their roles in response to EGF and ionizing radiation. EGF activated EGFRwt with no effect on EGFRvIII. In contrast, a single radiation exposure of 2 Gy resulted in a 2.8- and 4.3-fold increase in Tyr phosphorylation of EGFRwt and EGFRvIII, respectively. Downstream consequences of this radiation-induced activation were examined by inhibiting EGFRwt and EGFRvIII with AG1478 (kinase inhibitor). The radiation-induced 8.5-fold activation of the pro-proliferative mitogen-activated protein kinase and the 3.2-fold stimulation of the antiapoptotic AKT/phosphatidylinositol-3-kinase pathways by EGFRvIII far exceeded that in CHO.EGFR wt cells. Thus, based on colony formation and apoptosis assays, EGFRvIII expression conferred a stronger cytoprotective response to radiation than EGFRwt, resulting in relative radioresistance. Therefore, disabling EGFRvIII in addition to EGFRwt needs to be considered in any therapeutic approach aimed at targeting EGFR for tumor cell radiosensitization.

Indexed as

CytoprotectionProtein Serine-Threonine KinasesRadiation ToleranceAnimalsApoptosisCHO CellsCricetinaeEnzyme ActivationEpidermal Growth FactorErbB ReceptorsHumansMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktQuinazolinesAKT1 protein, humanEpidermal Growth Factorepidermal growth factor receptor VIIIErbB ReceptorsMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktQuinazolinesRTKI cpdTyrphostins

Identifiers

PMID12944901
OpenAlexW2050907629

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.