Evidence map›Paper›PMID 25373520›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Selective inhibition of tumor growth by clonal NK cells expressing an ErbB2/HER2-specific chimeric antigen receptor.

Kurt Schönfeld, Christiane Sahm, Congcong Zhang, Sonja Naundorf, Christian Brendel, Marcus Odendahl, Paulina Nowakowska, Halvard Bönig, Ulrike Köhl, Stephan Kloess and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers.

0numbers the graph read from it
0cells of the map it votes in
231citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

231 citing papers in PubMed, 338 citations in OpenAlex.

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  16. Tumor hypoxia shapes natural killer cell anticancer activities.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  17. Rendering NK Cells Antigen-Specific for the Therapy of Solid Tumours.International journal of molecular sciences · 2025
    Review
  18. Article
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  20. Article

171 more citing papers are in PubMed but not listed here.

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

22 authors at 7 institutions in 1 country.

Kurt SchönfeldGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Christiane SahmGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Congcong ZhangGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Sonja NaundorfEUFETS GmbH, Idar-Oberstein, Germany.
Christian BrendelGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Marcus OdendahlInstitute for Transfusion Medicine, German Red Cross Blood Donation Service North-East, Dresden and Transfusion Medicine, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany.
Paulina NowakowskaInstitute for Transfusion Medicine and Immunohematology, Goethe University, and German Red Cross Blood Donation Service Baden-Württemberg-Hessen, Frankfurt am Main, Germany.
Halvard BönigInstitute for Transfusion Medicine and Immunohematology, Goethe University, and German Red Cross Blood Donation Service Baden-Württemberg-Hessen, Frankfurt am Main, Germany.
Ulrike KöhlInstitute of Cellular Therapeutics, Hannover Medical School, Hannover, Germany.
Stephan KloessInstitute of Cellular Therapeutics, Hannover Medical School, Hannover, Germany.
Sylvia KöhlerGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Heidi Holtgreve-GrezInstitute of Human Genetics, University of Heidelberg, Heidelberg, Germany.
Anna JauchInstitute of Human Genetics, University of Heidelberg, Heidelberg, Germany.
Manfred SchmidtDepartment of Translational Oncology, National Center for Tumor Diseases and German Cancer Research Center, Heidelberg, Germany.
Ralf SchubertPediatric Pulmonology, Allergy and Cystic Fibrosis, University Hospital, Frankfurt am Main, Germany.
Klaus KühlckeEUFETS GmbH, Idar-Oberstein, Germany.
Erhard SeifriedInstitute for Transfusion Medicine and Immunohematology, Goethe University, and German Red Cross Blood Donation Service Baden-Württemberg-Hessen, Frankfurt am Main, Germany.
Hans G KlingemannConkwest Inc., Cardiff-by-the-Sea, California, USA.
Michael A Rieger1] Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany [2] Department of Hematology/Oncology, University Hospital, Frankfurt am Main, Germany [3] German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Torsten TonnInstitute for Transfusion Medicine, German Red Cross Blood Donation Service North-East, Dresden and Transfusion Medicine, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany.
Manuel GrezGeorg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Winfried S Wels1] Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany [2] German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Georg Speyer Haus · DEHeidelberg University · DEGerman Red Cross · DEMedizinische Hochschule Hannover · DEGoethe University Frankfurt · DETU Dresden · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells are an important effector cell type for adoptive cancer immunotherapy. Similar to T cells, NK cells can be modified to express chimeric antigen receptors (CARs) to enhance antitumor activity, but experience with CAR-engineered NK cells and their clinical development is still limited. Here, we redirected continuously expanding and clinically usable established human NK-92 cells to the tumor-associated ErbB2 (HER2) antigen. Following GMP-compliant procedures, we generated a stable clonal cell line expressing a humanized CAR based on ErbB2-specific antibody FRP5 harboring CD28 and CD3ζ signaling domains (CAR 5.28.z). These NK-92/5.28.z cells efficiently lysed ErbB2-expressing tumor cells in vitro and exhibited serial target cell killing. Specific recognition of tumor cells and antitumor activity were retained in vivo, resulting in selective enrichment of NK-92/5.28.z cells in orthotopic breast carcinoma xenografts, and reduction of pulmonary metastasis in a renal cell carcinoma model, respectively. γ-irradiation as a potential safety measure for clinical application prevented NK cell replication, while antitumor activity was preserved. Our data demonstrate that it is feasible to engineer CAR-expressing NK cells as a clonal, molecularly and functionally well-defined and continuously expandable cell therapeutic agent, and suggest NK-92/5.28.z cells as a promising candidate for use in adoptive cancer immunotherapy.

Indexed as

Gene ExpressionAnimalsBreast NeoplasmsCell Line, TransformedCell Line, TumorClonal EvolutionCytotoxicity, ImmunologicDisease Models, AnimalEpitopes, T-LymphocyteErb-b2 Receptor Tyrosine KinasesFemaleGenetic VectorsHumansImmunophenotypingImmunotherapyKiller Cells, NaturalEpitopes, T-LymphocyteErb-b2 Receptor Tyrosine KinasesReceptors, ImmunologicRecombinant Fusion Proteins

Identifiers

PMID25373520
PMCPMC4445620
OpenAlexW2016523043

What OpenQuestion holds

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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.