Evidence map›Paper›PMID 38259442›Full record

ArticleFrontiers in immunology2023

Chimeric antigen-receptor (CAR) engineered natural killer cells in a chronic myeloid leukemia (CML) blast crisis model.

Jusuf Imeri, Paul Marcoux, Matthias Huyghe, Christophe Desterke, Daianne Maciely Carvalho Fantacini, Frank Griscelli, Dimas T Covas, Lucas Eduardo Botelho de Souza, Annelise Bennaceur Griscelli, Ali G Turhan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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 4 institutions in 2 countries.

Jusuf ImeriINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Paul MarcouxINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Matthias HuygheINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Christophe DesterkeINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Daianne Maciely Carvalho FantaciniBlood Center of Ribeirão Preto/Ribeirão Preto School of Medicine/University of São Paulo, Ribeirao Preto, SP, Brazil.
Frank GriscelliINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Dimas T CovasBlood Center of Ribeirão Preto/Ribeirão Preto School of Medicine/University of São Paulo, Ribeirao Preto, SP, Brazil.
Lucas Eduardo Botelho de SouzaBlood Center of Ribeirão Preto/Ribeirão Preto School of Medicine/University of São Paulo, Ribeirao Preto, SP, Brazil.
Annelise Bennaceur GriscelliINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Ali G TurhanINSERM UMR-S-1310, Université Paris Saclay, Villejuif, France and ESTeam Paris Sud, Université Paris Saclay, Villejuif, France.
Inserm · FRUniversidade de São Paulo · BRUniversité Paris-Saclay · FRInstituto Butantan · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the last two decades, the introduction of tyrosine kinase inhibitors (TKIs) to the therapy has changed the natural history of CML but progression into accelerated and blast phase (AP/BP) occurs in 3-5% of cases, especially in patients resistant to several lines of TKIs. In TKI-refractory patients in advanced phases, the only curative option is hematopoietic stem cell transplantation. We and others have shown the relevance of the expression of the Interleukin-2-Receptor α subunit (IL2RA/CD25) as a biomarker of CML progression, suggesting its potential use as a therapeutic target for CAR-based therapies. Here we show the development of a CAR-NK therapy model able to target efficiently a blast crisis cell line (K562). The design of the CAR was based on the scFv of the clinically approved anti-CD25 monoclonal antibody (Basiliximab). The CAR construct was integrated into NK92 cells resulting in the generation of CD25 CAR-NK92 cells. Target K562 cells were engineered by lentiviral gene transfer of CD25.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, MyeloidReceptors, Chimeric AntigenAnimalsBlast CrisisHumansK562 CellsKiller Cells, NaturalMiceReceptors, Chimeric Antigenblast crisis CMLCAR-NKCD25leukemiaNK92

Identifiers

PMID38259442
PMCPMC10801069
OpenAlexW4390664771

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.