Evidence map›Paper›PMID 40313947›Full record

ArticleFrontiers in immunology2025

Multiplex immunophenotyping of human acute myeloid leukemia patients revealed single -cell heterogeneity with special attention on therapy sensitive and therapy resistant subpopulations.

Nikolett Gémes, Benedek Rónaszéki, Szabolcs Modok, Zita Borbényi, Imre Földesi, Éva Trucza, Blanka Godza, Zsuzsanna László, Balázs Csernus, László Krenács and 5 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

15 authors.

Nikolett Gémes *Laboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Center, Szeged, Hungary.
Benedek Rónaszéki *Department of Internal Medicine, Hematology Center, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Szabolcs ModokDepartment of Internal Medicine, Hematology Center, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Zita BorbényiDepartment of Internal Medicine, Hematology Center, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Imre FöldesiFaculty of Medicine, Institute of Laboratory Medicine, University of Szeged, Szeged, Hungary.
Éva TruczaFaculty of Medicine, Institute of Laboratory Medicine, University of Szeged, Szeged, Hungary.
Blanka GodzaDepartment of Medical Genetics, University of Szeged, Szeged, Hungary.
Zsuzsanna LászlóDepartment of Medical Genetics, University of Szeged, Szeged, Hungary.
Balázs Csernus1st Department of Pathology and Experimental Cancer Research, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
László KrenácsLaboratory of Tumor Pathology and Molecular Diagnostics, Szeged, Hungary.
Enikő BagdiLaboratory of Tumor Pathology and Molecular Diagnostics, Szeged, Hungary.
Enikő SzabóLaboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Center, Szeged, Hungary.
László G PuskásLaboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Center, Szeged, Hungary.
Valeria BertagnoloUniversity of Ferrara, Department of Morphology, Surgery and Experimental Medicine, Ferrara, Italy.
Gábor J SzebeniLaboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Center, Szeged, Hungary.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Understanding leukemia-associated immunophenotypes (LAIP) could assist in the design of therapies to ameliorate patient benefits in acute myeloid leukemia (AML). In our study, focusing on single-cell heterogeneity in therapeutic resistance, flow cytometric immunophenotyping of the peripheral blood of therapy-naive and follow-up AML patients versus age and sex-matched healthy controls (HCs) was performed. Methods: The FACS panel consisted of Viobility 405/520 Fixable Dye, Anti-human CD45, CD19, CD3, CD7, CD33, CD34, CD38, CD64, CD117, CD135, HLA-DR antibodies. Unsupervised clustering algorithms such as Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) and Flow cytometry data that builds Self-Organizing Maps (FlowSOM) were used to reveal the LAIP. The measurable residual disease (MRD) was monitored by our proposed manual gating. To complement the characterization of peripheral immune cells, Luminex MAGPIX was used to measure the concentration of 31 soluble immune-oncology mediators from the plasma of AML patients and HC. Results: Both manual gating, UMAP and FlowSOM showed normalization of LAIP similar to the HC immune landscape following therapy. Eleven metaclusters (MCs) were associated with AML before therapy. The follow-up of AML samples revealed four MCs of therapy sensitive cells, and one MC composed of therapeutic resistant cells (MC12: CD3-CD7-CD33-CD38- CD64- HLA-DR- CD117- CD135-) identified by the FlowSOM analysis. The initial AML blasts in the MRD gate (CD19-, CD45+, CD3-, CD38+/CD34±, CD7+/CD117+, CD117+/CD135+) were detectable at the lowest frequency in our current study at 22 cells per 100,000 (0.022%) CD45+CD3- living singlet parental population. In the plasma of AML patients the levels of BAFF, B7-H2, B7-H4, CD25, MICA, and Siglec-7 were increased versus HCs. Conclusions: This study focused on understanding the LAIP in AML before and after therapeutic intervention. The study highlights the potential of using single-cell LAIP profiling and immune mediator measurements to monitor therapy response and identify measurable residual disease and therapy resistant cell populations in AML.

Indexed as

Drug Resistance, NeoplasmImmunophenotypingLeukemia, Myeloid, AcuteAdultAgedAntigens, CDBiomarkers, TumorFemaleFlow CytometryHumansMaleMiddle AgedNeoplasm, ResidualSingle-Cell AnalysisAntigens, CDBiomarkers, Tumoracute myeloid leukemiadrug resistanceleukemia-associated immunophenotypeluminex MAGPIXminimal residual diseasesingle-cell immunophenotyping

Identifiers

PMID40313947
PMCPMC12043712

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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.