Evidence map›Paper›PMID 42397418›Full record

ArticleCancer immunology, immunotherapy : CII2026

EGFRxCD16 bispecific antibodies orchestrate superior NK cell-mediated lysis of ovarian cancer and NSCLC cell lines in combination with oncolytic viruses.

Sarah Gahbauer, Thomas Poiret

Abstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

2 authors.

Sarah GahbauerDepartment of Medicine Huddinge (MedH), Karolinska Institutet, Stockholm, Sweden.
Thomas PoiretDepartment of Medicine Huddinge (MedH), Karolinska Institutet, Stockholm, Sweden. thomas.poiret@ki.se.

Funding

Cancerfonden 2023-01988Swedish Medical Research Council 2021-01755The Swedish Childhood Cancer Fund PR2022-0066
6 · The paper itself

Abstract

Combination therapy integrating bispecific antibody (BsAb) and oncolytic viruses (OVs) to enhance antitumor immune response offers a promising therapeutic approach in comparison with OV treatment alone. This study aims to strengthen and characterize NK cell-mediated antitumor responses using modified oncolytic viruses, i.e., ONCOS-102 and ONCOS-204 genetically engineered to express Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) and the ligand of inducible T-cell co-stimulator (ICOSL), respectively, in combination with a BsAb targeting CD16 and the epidermal growth factor receptor (EGFR). Changes in phenotype, degranulation, cytokine production, and cytotoxicity of NK cells induced by combined treatment were compared with those induced by individual treatment strategies against non-small cell lung cancer, malignant melanoma, and ovarian cancer. Using flow cytometry and colorimetry-based cytotoxic assays, our results showed that EGFRxCD16 BsAb was the main variable in driving NK cells toward an activated phenotype and enhanced NK function; while the OVs alone did not demonstrate drastic impact on NK cells. Interestingly, tumor preconditioning with OVs in combination with EGFRxCD16 BsAb showed the most potent NK cytotoxicity in comparison with EGFRxCD16 BsAb alone and appeared to synergize best against ovarian and EGFRmut lung tumor cell lines. Despite differences between tumor types, our data suggest a favorable interplay between OVs, especially ONCOS-102, and EGFRxCD16 BsAb  in sensitizing NK cell antitumor response in vitro. These results warrant further in vivo exploration and clinical translation of this promising combination of therapeutic modalities.

Indexed as

Antibodies, BispecificCarcinoma, Non-Small-Cell LungKiller Cells, NaturalLung NeoplasmsOncolytic VirotherapyOncolytic VirusesOvarian NeoplasmsAnimalsCell Line, TumorCombined Modality TherapyCytotoxicity, ImmunologicErbB ReceptorsFemaleGPI-Linked ProteinsHumansReceptors, IgGAntibodies, BispecificEGFR protein, humanErbB ReceptorsGPI-Linked ProteinsReceptors, IgGBispecific antibodyCD16EGFRNK cellsOncolytic virus

Identifiers

PMID42397418
PMCPMC13332092

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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.