Evidence map›Paper›PMID 32541873›Full record

ArticleBritish journal of cancer2020

Cetuximab-induced natural killer cell cytotoxicity in head and neck squamous cell carcinoma cell lines: investigation of the role of cetuximab sensitivity and HPV status.

Hasan Baysal, Ines De Pauw, Hannah Zaryouh, Jorrit De Waele, Marc Peeters, Patrick Pauwels, Jan Baptist Vermorken, Evelien Smits, Filip Lardon, Julie Jacobs and 1 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

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  9. NK cells in HPV-related tumorigenesis: mechanisms and clinical applications.Frontiers in cellular and infection microbiology · 2025
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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.

Hasan BaysalCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium. hasan.baysal@uantwerpen.be.
Ines De PauwCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Hannah ZaryouhCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Jorrit De WaeleCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Marc PeetersCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Patrick PauwelsCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Jan Baptist VermorkenCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Evelien SmitsCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Filip LardonCenter for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
Julie Jacobs *Center for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
An Wouters *Center for Oncological Research (CORE), University of Antwerp, Antwerp, Belgium.
University of Antwerp · BEAntwerp University Hospital · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe epidermal growth factor receptor (EGFR) is overexpressed by 80-90% of squamous cell carcinoma of head and neck (HNSCC). In addition to inhibiting EGFR signal transduction, cetuximab, a monoclonal antibody targeting EGFR can also bind to fragment crystallisable domain of immunoglobulins G1 present on natural killer (NK), causing antibody-dependent cellular cytotoxicity (ADCC). However, presence of cetuximab resistance limits effective clinical management of HNSCC.

methodsIn this study, differences in induction of ADCC were investigated in a panel of ten HNSCC cell lines. Tumour cells were co-cultured with NK cells and monitored using the xCELLigence RTCA.

resultsWhile ADCC was not influenced by HPV status, hypoxia and cetuximab resistance did affect ADCC differentially. Intrinsic cetuximab-resistant cell lines showed an increased ADCC induction, whereas exposure to hypoxia reduced ADCC. Baseline EGFR expression was not correlated with ADCC. In contrast, EGFR internalisation following cetuximab treatment was positively correlated with ADCC.

conclusionThese findings support the possibility that resistance against cetuximab can be overcome by NK cell-based immune reactions. As such, it provides an incentive to combine cetuximab with immunotherapeutic approaches, thereby possibly enhancing the anti-tumoural immune responses and achieving greater clinical effectiveness of EGFR-targeting agents.

Indexed as

Antibody-Dependent Cell CytotoxicityAntineoplastic Agents, ImmunologicalCell Growth ProcessesCell Line, TumorCetuximabErbB ReceptorsHead and Neck NeoplasmsHumansKiller Cells, NaturalPapillomaviridaePapillomavirus InfectionsSquamous Cell Carcinoma of Head and NeckAntineoplastic Agents, ImmunologicalCetuximabEGFR protein, humanErbB Receptors

Identifiers

PMID32541873
PMCPMC7462851
OpenAlexW3035383735

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.