Evidence map›Paper›PMID 42392183›Full record

ReviewBlood advances2026

Minor histocompatibility antigen TCR-T.

Elizabeth F Krakow, Marie Bleakley

Abstract readReview
In one paragraph

Review in Blood advances, 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

2 authors.

Elizabeth F KrakowClinical Research Division, Fred Hutchinson Cancer Center, Seattle, WA.ORCID 0000-0002-2690-3799
Marie BleakleyTranslational Science and Therapeutics Division, Fred Hutchinson Cancer Center, Seattle, WA.ORCID 0000-0002-7018-8702

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractMinor histocompatibility antigens (MiHA) are polymorphic peptides presented by HLA molecules on recipient cells in allogeneic hematopoietic cell transplantation (allo-HCT) and are derived from proteins with genetic variants that differ between recipient and donor. After allo-HCT, hematopoietic-restricted MiHA enable selective targeting of residual recipient-derived hematopoiesis, including malignant cells. Advances in engineering T cells with high-affinity, MiHA-specific T-cell receptors (TCR; TCR-T) are enabling clinical translation of MiHA T-cell immunotherapy. Early-phase trials of HA-1- and HA-2-specific TCR-T demonstrate safety, persistence, and durable antileukemic activity in high-risk or relapsed disease. To accelerate translation, the field should expand TCR-T development to additional MiHA targets to broaden HLA and population coverage, integrate MiHA genotyping into donor selection, and devise platform trials to include patients with various MiHA/HLA genotypes and to efficiently test combination therapies. MiHA-directed TCR-T represents a genetically precise, potentially routine HCT adjunct that promises to fortify graft-versus-leukemia effects and improve relapse-free survival.

Indexed as

Minor Histocompatibility AntigensReceptors, Antigen, T-CellT-LymphocytesAnimalsHematopoietic Stem Cell TransplantationHumansTransplantation, HomologousMinor Histocompatibility AntigensReceptors, Antigen, T-Cell

Identifiers

PMID42392183
PMCPMC13578979

What OpenQuestion 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 OpenQuestion graph.