Evidence map›Paper›PMID 29603584›Full record

ArticleMolecular oncology2018

Simultaneous targeting of EGFR, HER2, and HER4 by afatinib overcomes intrinsic and acquired cetuximab resistance in head and neck squamous cell carcinoma cell lines.

Ines De Pauw, Filip Lardon, Jolien Van den Bossche, Hasan Baysal, Erik Fransen, Vanessa Deschoolmeester, Patrick Pauwels, Marc Peeters, Jan Baptist Vermorken, An Wouters

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-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

28 citing papers in PubMed, 48 citations in OpenAlex.

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  18. Deletion of p53 and Hyper-Activation of PIK3CA in Keratin-15International journal of molecular sciences · 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

10 authors at 3 institutions in 1 country.

Ines De PauwCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Filip LardonCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Jolien Van den BosscheCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Hasan BaysalCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Erik FransenStatUa Center for Statistics, University of Antwerp, Belgium.
Vanessa DeschoolmeesterCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Patrick PauwelsCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Marc PeetersCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
Jan Baptist VermorkenCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
An WoutersCenter for Oncological Research (CORE), University of Antwerp, Wilrijk, Belgium.
University of Antwerp · BEAntwerp University Hospital · BEStatistics Belgium · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR, HER1) is a therapeutic target in head and neck squamous cell carcinoma (HNSCC). After initial promising results with EGFR-targeted therapies such as cetuximab, therapeutic resistance has become a major clinical problem, and new treatment options are therefore necessary. Moreover, the relationship between HER receptors, anti-EGFR therapies, and the human papillomavirus (HPV) status in HNSCC is not fully understood. In contrast to first-generation EGFR inhibitors, afatinib irreversibly inhibits multiple HER receptors simultaneously. Therefore, treatment with afatinib might result in a more pronounced therapeutic benefit, even in patients experiencing cetuximab resistance. In this study, the cytotoxic effect of afatinib as single agent and in combination with cisplatin was investigated in cetuximab-sensitive, intrinsically cetuximab-resistant, and acquired cetuximab-resistant HNSCC cell lines with different HPV status under normoxia and hypoxia. Furthermore, the influence of cetuximab resistance, HPV, and hypoxia on the expression of HER receptors was investigated. Our results demonstrated that afatinib was able to establish cytotoxicity in cetuximab-sensitive, intrinsically cetuximab-resistant, and acquired cetuximab-resistant HNSCC cell lines, independent of the HPV status. However, cross-resistance between cetuximab and afatinib might be possible. Treatment with afatinib caused a G

Indexed as

AfatinibApoptosisCaspasesCell CycleCell HypoxiaCell Line, TumorCetuximabDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesErbB ReceptorsHumansInhibitory Concentration 50OxygenReceptor, ErbB-4Squamous Cell Carcinoma of Head and NeckAfatinibCaspasesCetuximabErb-b2 Receptor Tyrosine KinasesErbB ReceptorsOxygenReceptor, ErbB-4afatinibcetuximabepidermal growth factor receptorhead and neck squamous cell carcinomahuman papillomavirusresistance

Identifiers

PMID29603584
PMCPMC5983215
OpenAlexW2795117080

What OpenQuestion holds

Textmetadata
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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.