Evidence map›Paper›PMID 40853614›Full record

ArticleCurrent medical science2025

CD44v6 CAR-T Cells Target DNMT3A-Mutant AML: Synergistic Enhancement by Decitabine.

Hui-Min Li, Yi-Mei Que, Xiao-Ya Cai, Ping-Fan Lu, Li-Man Lin, Min Xiao, Li Zhu, Deng-Ju Li

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Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

  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

8 authors.

Hui-Min Li *Department of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Yi-Mei Que *Department of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiao-Ya CaiDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Ping-Fan LuDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Li-Man LinDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Min XiaoDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Li ZhuDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China.
Deng-Ju LiDepartment of Hematology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, China. lidengju@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0001-7629-2642

Funding

Chen Xiaoping Foundation for the development of Science and Technology of Hubei Province CXPJJH122001-2221the National Natural Science Foundation of China 82270177
6 · The paper itself

Abstract

objectiveAcute myeloid leukemia (AML) is a highly heterogeneous disease, and molecular events such as DNMT3A gene mutations are associated with poor prognosis in AML patients. Consequently, there is an urgent need for a novel therapeutic approach for AML.

methodsDNMT3A mRNA and protein expression were confirmed in DNMT3A-mutant AML cells via RT-qPCR and Western blotting. Cell proliferation and apoptosis were assessed via CCK-8 and Annexin V/PI staining, respectively. Flow cytometry was used to analyze surface antigens and CD44v6 CAR-T-cell transfection efficiency. CD44v6-directed CAR plasmids were constructed, and lentiviruses were packaged. Methylation-specific PCR was used to evaluate differences in promoter methylation, whereas ELISA was used to measure cytokine secretion.

resultsIn this study, we found that the DNMT3A-mutant group presented significantly increased expression of CD44v6 on the cell surface. Methylation of the CD44 promoter region was lower in the mutant group than in the control group. CD44v6 CAR-T cells exhibited specific cytotoxicity against DNMT3A-mutant AML cells. Furthermore, pretreatment with low concentrations of decitabine significantly enhanced the killing effect of CD44v6 CAR-T cells on DNMT3A-mutant AML cells (P < 0.05). Additionally, decitabine treatment upregulated the expression of CD44v6 on the surface of DNMT3A-mutant AML cells (P < 0.05).

conclusionCD44v6 is a promising CAR-T-cell therapy target in AML patients with DNMT3A mutations. Notably, treatment with decitabine resulted in increased CD44v6 expression on the cell surface of DNMT3A-mutant AML cells. This increase in CD44v6 expression facilitates improved recognition and targeting by CD44v6 CAR-T cells.

Indexed as

DecitabineDNA (Cytosine-5-)-MethyltransferasesHyaluronan ReceptorsImmunotherapy, AdoptiveLeukemia, Myeloid, AcuteReceptors, Chimeric AntigenApoptosisCell Line, TumorCell ProliferationDNA MethylationDNA Methyltransferase 3AHumansMutationPromoter Regions, GeneticDecitabineDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanHyaluronan ReceptorsReceptors, Chimeric AntigenAcute myeloid leukemiaCD44v6Chimeric antigen receptorCombination therapyDecitabineDNA methylationDNMT3A mutationEpigenetic regulation

Identifiers

PMID40853614

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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.