Evidence map›Paper›PMID 23830194›Full record

ReviewRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology2013

Nuclear EGFR as a molecular target in cancer.

Toni M Brand, Mari Iida, Neha Luthar, Megan M Starr, Evan J Huppert, Deric L Wheeler

Erratum issuedAbstract readReview
In one paragraph

Review in Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 134 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 3 pooled it
15.9field-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

134 citing papers in PubMed, 3 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. EGFR expression and survival in patients given cetuximab and chemoradiation for stage III non-small cell lung cancer: a secondary analysis of RTOG 0324.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2014
    Trial
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  7. Review
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  10. Beyond the membrane: rethinking EGFR signaling in physiology and cancer.Cellular and molecular life sciences : CMLS · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Toni M BrandDepartment of Human Oncology, University of Wisconsin School of Medicine and Public Health, Wisconsin Institute for Medical Research, Madison, USA.
Mari Iida
Neha Luthar
Megan M Starr
Evan J Huppert
Deric L Wheeler
Institute for Medical Research · USWisconsin Institutes for Discovery · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
NCATS NIH HHS UL1 TR000427NCI NIH HHS P30 CA014520NIGMS NIH HHS T32 GM081061
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) has been one of the most targeted receptors in the field of oncology. While anti-EGFR inhibitors have demonstrated clinical success in specific cancers, most patients demonstrate either intrinsic or acquired resistance within one year of treatment. Many mechanisms of resistance to EGFR inhibitors have been identified, one of these being attributed to alternatively localized EGFR from the cell membrane into the cell's nucleus. Inside the nucleus, EGFR functions as a co-transcription factor for several genes involved in cell proliferation and angiogenesis, and as a tyrosine kinase to activate and stabilize proliferating cell nuclear antigen and DNA dependent protein kinase. Nuclear localized EGFR is highly associated with disease progression, worse overall survival in numerous cancers, and enhanced resistance to radiation, chemotherapy, and the anti-EGFR therapies gefitinib and cetuximab. In this review the current knowledge of how nuclear EGFR enhances resistance to cancer therapeutics is discussed, in addition to highlighting ways to target nuclear EGFR as an anti-cancer strategy in the future.

Indexed as

AnimalsCelecoxibCell Line, TumorDrug Resistance, NeoplasmErbB ReceptorsHumansNeoplasmsProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktPyrazolesRadiation ToleranceSulfonamidesCelecoxibErbB ReceptorsProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktPyrazolesSulfonamidesBCRPbreast cancer resistant proteinCancerCOX-2cyclooxygenase-2DNA-PKDNA protein kinaseEGFRepidermal growth factor receptorhead and neck squamous cell carcinomaHNSCCINMinner nuclear membraneiNOSlatent membrane protein 1LMP1MUC1mucin-1nitric oxide synthaseNLSnon-small cell lung cancerNPCNSLCNuclear EGFRnuclear localization sequencenuclear localization signalnuclear pore complexONMouter nuclear membranePCNAPNPasepolynucleotide phosphorylaseproliferating cell nuclear antigenResistanceRHARNA helicase ATAT interacting proteinTIF2TIP3TKITNBCtranscriptional intermediary factor 2triple negative breast cancertyrosine kinase inhibitor

Identifiers

PMID23830194
PMCPMC3818450
OpenAlexW2044151404

What OpenQuestion holds

Textmetadata
LicenceTDM
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.