Evidence map›Paper›PMID 38637557›Full record

ArticleBlood cancer journal2024

Induction of NK cell reactivity against acute myeloid leukemia by Fc-optimized CD276 (B7-H3) antibody.

Sylwia A Stefańczyk, Ilona Hagelstein, Martina S Lutz, Stefanie Müller, Samuel J Holzmayer, Grace Jarjour, Latifa Zekri, Jonas S Heitmann, Helmut R Salih, Melanie Märklin

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

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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 1 institution in 1 country.

Sylwia A StefańczykClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.ORCID 0000-0002-4134-4171
Ilona HagelsteinClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Martina S LutzClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Stefanie MüllerClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Samuel J HolzmayerClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.ORCID 0009-0006-4513-2367
Grace JarjourClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Latifa ZekriClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Jonas S HeitmannClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Helmut R SalihClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
Melanie MärklinClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany. Melanie.Maerklin@med.uni-tuebingen.de.ORCID 0000-0002-2920-3894
Deutschen Konsortium für Translationale Krebsforschung · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) MA 9302/2-1Deutsche Krebshilfe (German Cancer Aid) 70113496
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) remains a therapeutic challenge despite recent therapeutic advances. Although monoclonal antibodies (mAbs) engaging natural killer (NK) cells via antibody-dependent cellular cytotoxicity (ADCC) hold promise in cancer therapy, almost none have received clinical approval for AML, so far. Recently, CD276 (B7-H3) has emerged as a promising target for AML immunotherapy, due to its high expression on leukemic blasts of AML patients. Here, we present the preclinical development of the Fc-optimized CD276 mAb 8H8_SDIE with enhanced CD16 affinity. We demonstrate that 8H8_SDIE specifically binds to CD276 on AML cell lines and primary AML cells and induces pronounced NK cell activation and degranulation as measured by CD69, CD25, and CD107a. Secretion of IFNγ, TNF, granzyme B, granulysin, and perforin, which mediate NK cell effector functions, was induced by 8H8_SDIE. A pronounced target cell-restricted lysis of AML cell lines and primary AML cells was observed in cytotoxicity assays using 8H8_SDIE. Finally, xenograft models with 8H8_SDIE did not cause off-target immune activation and effectively inhibited leukemia growth in vivo. We here present a novel attractive immunotherapeutic compound that potently induces anti-leukemic NK cell reactivity in vitro and in vivo as treatment option for AML.

Indexed as

Killer Cells, NaturalLeukemia, Myeloid, AcuteAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityB7 AntigensHumansAntibodies, MonoclonalB7 AntigensCD276 protein, human

Identifiers

PMID38637557
PMCPMC11026476
OpenAlexW4394922338

What OpenQuestion holds

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LicenceCC BY
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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.