ArticleFunctional & integrative genomics2026
YTHDF1-ALYREF axis enhances mrna stability and tumor immune evasion in paediatric B-cell acute lymphoblastic leukemia.
Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Escorting mRNAs - the multifunctional and divergent roles of cap-chaperones in post-transcriptional gene expression.Journal of cell science · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Immune evasion mechanisms in paediatric B-cell acute lymphoblastic leukemia (B-ALL) hinder the efficacy of immunotherapies. Epitranscriptomic regulators such as m6A readers may modulate immune landscapes in B-ALL, but their roles remain poorly defined. Transcriptomic analysis of paediatric B-ALL samples highlighted YTHDF1 and ALYREF as co-upregulated candidates. Functional studies in YTHDF1-silenced B-ALL cells assessed ALYREF mRNA stability, PD-L1 expression, and migratory capacity. NSG xenograft models were used to investigate immune cell infiltration profiles. YTHDF1 enhanced ALYREF mRNA stability via binding to m6A-modified transcripts, promoting downstream PD-L1 expression. Knockdown of YTHDF1 led to significant reductions in ALYREF (60%) and PD-L1, accompanied by a 50% reduction in cell migration. Notably, CD8 + T cell infiltration in xenografts increased 2.5-fold, indicating improved tumor immunogenicity. The YTHDF1–ALYREF–PD-L1 axis represents a novel immune evasion mechanism in B-ALL. Therapeutic disruption of this pathway may restore T cell-mediated cytotoxicity and enhance the efficacy of existing immunotherapies.
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Registered trials
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.