Evidence map›Paper›PMID 31181683›Full record

ArticleCancers2019

An Fc-Optimized CD133 Antibody for Induction of Natural Killer Cell Reactivity against Colorectal Cancer.

Bastian J Schmied, Fabian Riegg, Latifa Zekri, Ludger Grosse-Hovest, Hans-Jörg Bühring, Gundram Jung, Helmut R Salih

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 23 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

7 authors at 2 institutions in 1 country.

Bastian J SchmiedClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), 72076 Partner site Tuebingen, Germany. Bastian.Schmied@med.uni-tuebingen.de.
Fabian RieggClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), 72076 Partner site Tuebingen, Germany. Fabian.Riegg@med.uni-tuebingen.de.
Latifa ZekriClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), 72076 Partner site Tuebingen, Germany. l.zekri-metref@dkfz.de.
Ludger Grosse-HovestDepartment for Immunology, Eberhard Karls University, 72076 Tuebingen, Germany. grosse-hovest@synimmune.de.
Hans-Jörg BühringDepartment of Hematology and Oncology, Eberhard Karls University, 72076 Tuebingen, Germany. gundram.jung@uni-tuebingen.de.
Gundram JungDepartment for Immunology, Eberhard Karls University, 72076 Tuebingen, Germany. hans-joerg.buehring@uni-tuebingen.de.
Helmut R SalihClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), 72076 Partner site Tuebingen, Germany. Helmut.Salih@med.uni-tuebingen.de.
University of Tübingen · DEGerman Cancer Research Center · DE

Funding

Deutsche Forschungsgemeinschaft SA1360/7-3Deutsche Forschungsgemeinschaft SA1360/9-1Deutsche Krebshilfe 111828Deutsche Krebshilfe 70112914Germany´s Excellence Strategy EXC 2180/1Wilhelm Sander-Stiftung 2007.115.3
6 · The paper itself

Abstract

The introduction of monoclonal antibodies (mAbs) has largely improved treatment options for cancer patients. The ability of antitumor mAbs to elicit antibody-dependent cellular cytotoxicity (ADCC) contributes to a large extent to their therapeutic efficacy. Many efforts accordingly aim to improve this important function by engineering mAbs with Fc parts that display enhanced affinity to the Fc receptor CD16 expressed, e.g., on natural killer (NK) cells. Here we characterized the CD133 mAb 293C3-SDIE that contains an engineered Fc part modified by the amino acid exchanges S239D/I332E-that reportedly increase the affinity to CD16-with regard to its ability to induce NK reactivity against colorectal cancer (CRC). 293C3-SDIE was found to be a stable protein with favorable binding characteristics achieving saturating binding to CRC cells at concentrations of approximately 1 µg/mL. While not directly affecting CRC cell growth and viability, 293C3-SDIE potently induced NK cell activation, degranulation, secretion of Interferon-γ, as well as ADCC resulting in potent lysis of CRC cell lines. Based on the preclinical characterization presented in this study and the available data indicating that CD133 is broadly expressed in CRC and represents a negative prognostic marker, we conclude that 293C3-SDIE constitutes a promising therapeutic agent for the treatment of CRC and thus warrants clinical evaluation.

Indexed as

ADCCantibodyCD133colorectal cancerimmunotherapyNK cellsprominin-1

Identifiers

PMID31181683
PMCPMC6627285
OpenAlexW2948695921

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.