Evidence mapPaperPMID 42440668Full record

ReviewFrontiers in immunology2026

Modulating CAR-T cell exhaustion and fitness in acute myeloid leukemia: mechanistic metabolic and microenvironmental strategies.

Erden Atilla

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Erden AtillaDivision of Transplantation and Cellular Therapy, Sylvester Comprehensive Cancer Center, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chimeric antigen receptor (CAR) T-cell therapy has achieved transformative outcomes in B-cell malignancies but remains limited in acute myeloid leukemia (AML), where antigenic heterogeneity, a suppressive myeloid-driven microenvironment, and a metabolically restrictive bone marrow niche collectively impair efficacy. In AML, CAR T-cell failure is driven not only by antigen escape but by a coordinated program of exhaustion encompassing transcriptional, epigenetic, metabolic, and functional dysfunction. The AML bone marrow niche further enforces dysfunction through suppressive immune populations, inhibitory cytokines, checkpoint signaling, metabolic competition, and impaired trafficking. This review outlines a "fitness-first" framework consolidating intrinsic and extrinsic determinants of CAR T-cell performance. Optimized manufacturing, cellular programming, and microenvironmental modulation provide a unified strategy to enhance CAR T-cell fitness and enable durable therapeutic responses in AML.

Indexed as

Immunotherapy, AdoptiveLeukemia, Myeloid, AcuteReceptors, Chimeric AntigenT-LymphocytesTumor MicroenvironmentAnimalsEpigenesis, GeneticHumansT-Cell ExhaustionReceptors, Chimeric AntigenAMLCAR T-cell engineeringCAR T-cell exhaustionepigenetic regulationmetabolic fitnessmicroenvironmentmitochondrial function

Identifiers

PMID42440668
PMCPMC13333761

What Socratic holds

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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 Socratic graph.