Evidence map›Paper›PMID 33561014›Full record

ArticleThe Journal of clinical investigation2021

Augmented antibody-based anticancer therapeutics boost neutrophil cytotoxicity.

Niels Heemskerk, Mandy Gruijs, A Robin Temming, Marieke H Heineke, Dennis Y Gout, Tessa Hellingman, Cornelis W Tuk, Paula J Winter, Suzanne Lissenberg-Thunnissen, Arthur Eh Bentlage and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

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  15. Activated neutrophils: A next generation cellular immunotherapy.Bioengineering & translational medicine · 2025
    Review
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  20. New immune cell engagers for cancer immunotherapy.Nature reviews. Immunology · 2024
    Review
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

17 authors at 5 institutions in 2 countries.

Niels HeemskerkAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Mandy GruijsAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
A Robin TemmingSanquin Research and Landsteiner Laboratory, Department of Experimental Immunohematology, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
Marieke H HeinekeAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Dennis Y GoutAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Tessa HellingmanAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Surgery, Cancer Center Amsterdam, De Boelelaan 1117, Amsterdam, Netherlands.
Cornelis W TukAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Paula J WinterAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Suzanne Lissenberg-ThunnissenSanquin Research and Landsteiner Laboratory, Department of Experimental Immunohematology, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
Arthur Eh BentlageSanquin Research and Landsteiner Laboratory, Department of Experimental Immunohematology, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
Marco de DonatisAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Marijn BögelsAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Thies RösnerSection for Stem Cell Transplantation and Immunotherapy, Department of Medicine II, Christian Albrechts University and University Hospital Schleswig Holstein, Kiel, Germany.
Thomas ValeriusSection for Stem Cell Transplantation and Immunotherapy, Department of Medicine II, Christian Albrechts University and University Hospital Schleswig Holstein, Kiel, Germany.
Jantine E BakemaAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Otolaryngology/Head-Neck Surgery, Cancer Center Amsterdam, De Boelelaan 1117, Amsterdam, Netherlands.
Gestur VidarssonSanquin Research and Landsteiner Laboratory, Department of Experimental Immunohematology, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
Marjolein van EgmondAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Cancer Center Amsterdam, Amsterdam Infection and Immunity, De Boelelaan 1117, Amsterdam, Netherlands.
Amsterdam Neuroscience · NLSanquin · NLChristian-Albrechts-Universität zu Kiel · DEAmsterdam University Medical Centers · NLVrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most clinically used anticancer mAbs are of the IgG isotype, which can eliminate tumor cells through NK cell-mediated antibody-dependent cellular cytotoxicity and macrophage-mediated antibody-dependent phagocytosis. IgG, however, ineffectively recruits neutrophils as effector cells. IgA mAbs induce migration and activation of neutrophils through the IgA Fc receptor (FcαRI) but are unable to activate NK cells and have poorer half-life. Here, we combined the agonistic activity of IgG mAbs and FcαRI targeting in a therapeutic bispecific antibody format. The resulting TrisomAb molecules recruited NK cells, macrophages, and neutrophils as effector cells for eradication of tumor cells in vitro and in vivo. Moreover, TrisomAb had long in vivo half-life and strongly decreased B16F10gp75 tumor outgrowth in mice. Importantly, neutrophils of colorectal cancer patients effectively eliminated tumor cells in the presence of anti-EGFR TrisomAb but were less efficient in mediating killing in the presence of IgG anti-EGFR mAb (cetuximab). The clinical application of TrisomAb may provide potential alternatives for cancer patients who do not benefit from current IgG mAb therapy.

Indexed as

AnimalsAntibodies, BispecificAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityAntigens, CDAntineoplastic Agents, ImmunologicalCell Line, TumorCetuximabFemaleHCT116 CellsHumansImmunoglobulin GKiller Cells, NaturalMacrophagesMaleMelanoma, ExperimentalAntibodies, BispecificAntibodies, MonoclonalAntigens, CDAntineoplastic Agents, ImmunologicalCetuximabFc(alpha) receptorImmunoglobulin GReceptors, FcImmunoglobulinsNeutrophilsTherapeutics

Identifiers

PMID33561014
PMCPMC7954609
OpenAlexW3126854146

What OpenQuestion holds

Textmetadata
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Registered trials

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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.