ArticleNature communications2025
miR-142 deficit in T cells during blast crisis promotes chronic myeloid leukemia immune escape.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed.
- Genomic context of mutations in MIR142 in blood cancers: summary and integrative analysis.Cellular & molecular biology letters · 2026Review
- Loss of endothelial miR-126 drives age-related decline in hematopoiesis.Haematologica · 2026Article
- Review
- NBSR: a Negative Binomial Softmax Regression model for microRNA-seq data analysis.Biostatistics (Oxford, England) · 2026Article
- MicroRNA-142 improves IL1RAP CAR-T cell activity in acute myeloid leukemia.Journal of hematology & oncology · 2025Article
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Authors and funding
29 authors.
Funding
Abstract
We reported that an acquired miR-142 deficit transforms chronic phase (CP) chronic myeloid leukemia (CML) leukemic stem cells (LSCs) into blast crisis (BC) LSCs. Given the role of miR-142 in the development and activity of the immune system, we postulated that this deficit also promotes LSC immune escape. Herein, we report on IL-6-driven miR-142 deficit occurring in T cells during BC transformation. In CML murine models, miR-142 deficit impairs thymic differentiation of lymphoid-primed multipotent progenitors (LMPP) into T cells and prevents T cells' metabolic reprogramming, thereby leading to loss of T cells and leukemia immune escape. Correcting miR-142 deficit with a miR-142 mimic compound (M-miR-142), alone or in combination with immune checkpoint antibodies, restores T cell number and immune activity, leading to LSC elimination and prolonged survival of BC CML murine and patient-derived xenograft models. These observations may open new therapeutic opportunities for BC CML and other myeloid malignancies.
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Registered trials
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