Evidence map›Paper›PMID 33915811›Full record

ArticleCancers2021

An Fc-Optimized CD133 Antibody for Induction of NK Cell Reactivity against B Cell Acute Lymphoblastic Leukemia.

Fabian Riegg, Martina S Lutz, Bastian J Schmied, Jonas S Heitmann, Manon Queudeville, Peter Lang, Gundram Jung, Helmut R Salih, Melanie Märklin

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Can CD133 Be Regarded as a Prognostic Biomarker in Oncology: Pros and Cons.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Review
  6. Article
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

9 authors at 3 institutions in 1 country.

Fabian RieggClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Martina S LutzClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Bastian J SchmiedClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Jonas S HeitmannClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Manon QueudevilleDepartment I-General Pediatrics, Children's Hospital, University Hospital Tübingen, Hematology/Oncology, 72076 Tuebingen, Germany.ORCID 0000-0002-5642-1846
Peter LangDepartment I-General Pediatrics, Children's Hospital, University Hospital Tübingen, Hematology/Oncology, 72076 Tuebingen, Germany.
Gundram JungDepartment for Immunology, Eberhard Karls University, 72076 Tuebingen, Germany.
Helmut R SalihClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0002-6719-1847
Melanie MärklinClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0002-2920-3894
German Cancer Research Center · DEUniversity Children's Hospital Tübingen · DEUniversity of Tübingen · DE

Funding

Deutsche Forschungsgemeinschaft SA 1360/9-3Deutsche Krebshilfe 70112914Deutsche Krebshilfe 70113496Deutsche Krebshilfe 70113999Germany's Excellence Strategy EXC 2180 390900677Wilhelm Sander-Stiftung 2017.100.3
6 · The paper itself

Abstract

In recent decades, antibody-dependent cellular cytotoxicity (ADCC)-inducing monoclonal antibodies (mAbs) have revolutionized cancer immunotherapy, and Fc engineering strategies have been utilized to further improve efficacy. A promising option is to enhance the affinity of an antibody's Fc-part to the Fc-receptor CD16 by altering the amino acid sequence. Herein, we characterized an S239D/I332E-modified CD133 mAb termed 293C3-SDIE for treatment of B cell acute lymphoblastic leukemia (B-ALL). Flow cytometric analysis revealed CD133 expression on B-ALL cell lines and leukemic cells of 50% (14 of 28) B-ALL patients. 293C3-SDIE potently induced NK cell reactivity against the B-ALL cell lines SEM and RS4;11, as well as leukemic cells of B-ALL patients in a target antigen-dependent manner, as revealed by analysis of NK cell activation, degranulation, and cytotoxicity. Of note, CD133 expression did not correlate with BCR-ABL, CD19, CD20, or CD22, which are presently used as therapeutic targets in B-ALL, which revealed CD133 as an independent target for B-ALL treatment. Increased CD133 expression was also observed in MLL-AF4-rearranged B-ALL, indicating that 293C3-SDIE may constitute a particularly suitable treatment option in this hard-to-treat subpopulation. Taken together, our results identify 293C3-SDIE as a promising therapeutic agent for the treatment of B-ALL.

Indexed as

acute lymphoblastic leukemiaADCCB-ALLCD133Fc engineeringimmunotherapyNK cellsprominin-1

Identifiers

PMID33915811
PMCPMC8036612
OpenAlexW3152114754

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.