Evidence map›Paper›PMID 41888396›Full record

ArticleLeukemia2026

Synergizing hypomethylating agents with off-the-shelf CD70-targeted chimeric antigen receptor-engineered natural killer T cells for the treatment of acute myeloid leukemia.

Yan-Ruide Li, Xinyuan Shen, Yuning Chen, Yichen Zhu, Jie Huang, Caspian Oliai, Lili Yang

Abstract read
In one paragraph

Article in Leukemia, 2026. 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
–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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Frontiers in pharmacology · 2026
    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

7 authors.

Yan-Ruide LiDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-9858-300X
Xinyuan ShenDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA.
Yuning ChenDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA.
Yichen ZhuDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA.
Jie HuangDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA.
Caspian OliaiDivision of Hematology-Oncology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Lili YangDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, USA. liliyang@ucla.edu.ORCID http://orcid.org/0000-0001-6568-0404

Funding

California Institute for Regenerative Medicine (CIRM) DISC2-11157California Institute for Regenerative Medicine (CIRM) DISC2-13015California Institute for Regenerative Medicine (CIRM) TRAN1-12250California Institute for Regenerative Medicine (CIRM) TRAN1-16050UC | University of California, Los Angeles (UCLA) CIRM-BSCRC Postdoctoral FellowshipUC | University of California, Los Angeles (UCLA) UCLA Chancellor's Award for Postdoctoral ResearchUC | University of California, Los Angeles (UCLA) UCLA Goodman-Luskin Microbiome Center Collaborative Research Fellowship AwardUC | University of California, Los Angeles (UCLA) UCLA MIMG M. John Pickett Post-Doctoral Fellow AwardUC | University of California, Los Angeles (UCLA) UCLA Sydney Finegold Postdoctoral Award
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the uncontrolled expansion of undifferentiated myeloid precursors in the bone marrow. Hypomethylating agents (HMAs) such as azacitidine and decitabine can reverse abnormal DNA methylation, promote leukemic cell differentiation, and enhance immune recognition, yet relapse and therapeutic resistance remain major challenges. In this study, we found that long-term, low-dose HMA treatment upregulated CD70, NK receptor ligands, and CD1d on AML tumor cells, rendering them more susceptible to chimeric antigen receptor (CAR)-engineered invariant natural killer T (CAR-NKT) cell-mediated cytotoxicity. To exploit these features, we generated two types of CD70-targeting CAR-NKT cells: cord blood hematopoietic stem and progenitor cell (HSPC)-derived allogeneic CAR70-NKT (

Indexed as

Antimetabolites, AntineoplasticCD27 LigandImmunotherapy, AdoptiveLeukemia, Myeloid, AcuteNatural Killer T-CellsReceptors, Chimeric AntigenAnimalsAzacitidineDecitabineDNA MethylationFemaleHumansMiceMice, Inbred NODMice, SCIDXenograft Model Antitumor AssaysAntimetabolites, AntineoplasticAzacitidineCD27 LigandCD70 protein, humanDecitabineReceptors, Chimeric Antigen

Identifiers

PMID41888396
PMCPMC13149322

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.