Evidence map›Paper›PMID 20622897›Full record

ArticleOncogene2010

Epidermal growth factor receptor variant III mediates head and neck cancer cell invasion via STAT3 activation.

S E Wheeler, S Suzuki, S M Thomas, M Sen, R J Leeman-Neill, S I Chiosea, C-T Kuan, D D Bigner, W E Gooding, S Y Lai and 1 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 101 citations in OpenAlex.

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  18. Mechanisms of resistance in head and neck cancer.American journal of cancer research · 2020
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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

11 authors at 2 institutions in 1 country.

S E WheelerDepartment of Otolaryngology, University of Pittsburgh and University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
S Suzuki
S M Thomas
M Sen
R J Leeman-Neill
S I Chiosea
C-T Kuan
D D Bigner
W E Gooding
S Y Lai
J R Grandis
UPMC Hillman Cancer Center · USDuke University Hospital · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2004 to 2026
$49.6M
Virus Production and Manipulation of Protein/Gene Expression ModuleP30EY008098 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Ethan A Rossi · 1989 to 2026
$17.8M
BRAIN TUMORS: IMMUNOLOGICAL AND BIOLOGICAL STUDIESR37CA011898 · NCI · DUKE UNIVERSITY · PI BIGNER, DARELL D · 1988 to 2012
$8.1M
STAT-Mediated TGFalpha EGFR Signaling in squamous cell carcinoma of head neckR01CA077308 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRANDIS, JENNIFER RUBIN · 1998 to 2018
$5.0M
Stat3 as a Therapeutic Target in Head and Neck CancerR01CA101840 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRANDIS, JENNIFER RUBIN · 2004 to 2008
$1.3M
NCI NIH HHS P50 CA097190NCI NIH HHS R01 CA077308NCI NIH HHS R01 CA101840NCI NIH HHS R01 CA77308NCI NIH HHS R37 CA011898NEI NIH HHS EY08098NEI NIH HHS P30 EY008098
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) is frequently overexpressed in head and neck squamous cell carcinoma (HNSCC) where aberrant signaling downstream of this receptor contributes to tumor growth. EGFR variant III (EGFRvIII) is the most commonly altered form of EGFR and contains a truncated ligand-binding domain. We previously reported that EGFRvIII is expressed in up to 40% of HNSCC tumors where it is associated with increased proliferation, tumor growth and chemoresistance to antitumor drugs including the EGFR-targeting monoclonal antibody cetuximab. Cetuximab was FDA-approved in 2006 for HNSCC but has not been shown to prevent invasion or metastasis. This study was undertaken to evaluate the mechanisms of EGFRvIII-mediated cell motility and invasion in HNSCC. We found that EGFRvIII induced HNSCC cell migration and invasion in conjunction with increased signal transducer and activator of transcription 3 (STAT3) activation, which was not abrogated by cetuximab treatment. Further investigation showed that EGF-induced expression of the STAT3 target gene HIF1-α, was abolished by cetuximab in HNSCC cells expressing wild-type EGFR under hypoxic conditions, but not in EGFRvIII-expressing HNSCC cells. These results suggest that EGFRvIII mediates HNSCC cell migration and invasion by increased STAT3 activation and induction of HIF1-α, which contribute to cetuximab resistance in EGFRvIII-expressing HNSCC tumors.

Indexed as

Neoplasm InvasivenessCarcinoma, Squamous CellErbB ReceptorsHead and Neck NeoplasmsHumansSTAT3 Transcription FactorErbB ReceptorsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID20622897
PMCPMC2940981
OpenAlexW1995828194

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.