Evidence map›Paper›PMID 12947392›Full record

ReviewOncogene2003

ERBB receptor tyrosine kinases and cellular radiation responses.

Rupert K Schmidt-Ullrich, Joseph N Contessa, Guido Lammering, George Amorino, Peck-Sun Lin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  14. Article
  15. AXL Is a Logical Molecular Target in Head and Neck Squamous Cell Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 2 countries.

Rupert K Schmidt-UllrichRadiation Oncology Department, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA. rullrich@hsc.vcu.edu
Joseph N Contessa
Guido Lammering
George Amorino
Peck-Sun Lin
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 P01CA72955NCI NIH HHS R01CA65896
6 · The paper itself

Abstract

Ionizing radiation induces in autocrine growth-regulated carcinoma and malignant glioma cells powerful cytoprotective responses that confer relative resistance to consecutive radiation exposures. Understanding the mechanisms of these responses should provide new molecular targets for tumor radiosensitization. ERBB and other receptor Tyr kinases have been identified as immediate early response gene products that are activated by radiation within minutes, as by their physiological growth factor ligands, and induce secondary stimulation of cytoplasmic protein kinase cascades. The simultaneous activation of all receptor Tyr kinases and nonreceptor Tyr kinases leads to complex cytoprotective responses including increased cell proliferation, reduced apoptosis and enhanced DNA repair. Since these responses contribute to cellular radioresistance, ERBB1, the most extensively studied ERBB receptor, is examined as a target for tumor cell radiosensitization. The three methods of ERBB1 inhibition include blockade of growth factor binding by monoclonal antibody against the ligand-binding domain, inhibition of the receptor Tyr kinase-mediating receptor activation, and overexpression of a dominant-negative epidermal growth factor receptor-CD533 that lacks the COOH-terminal 533 amino acids and forms nonfunctional heterodimeric complexes with wild-type receptors. All the three approaches enhance radiation toxicity in vitro and in vivo. The different mechanisms of inhibition have contributed to the understanding of cellular responses to radiation, vary in relative effectiveness and pose different challenges for translation.

Indexed as

AnimalsHumansNeoplasmsReceptor Protein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases

Identifiers

PMID12947392
OpenAlexW2029320277

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.