ArticleLeukemia2026
Targeting the eIF4F translation initiation complex disrupts BCR::ABL1 translation and overcomes drug resistance in CML.
Article in Leukemia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
12 authors.
Funding
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Abstract
Chronic myeloid leukemia (CML) is driven by the constitutively active BCR::ABL1 kinase, which promotes uncontrolled cell proliferation. Although protein-tyrosine kinase inhibitors (TKIs) have revolutionized CML treatment, resistance remains a significant barrier to curative therapy, particularly due to BCR::ABL1 mutations and the persistence of leukemia stem cells (LSCs). New treatment strategies that directly inhibit BCR::ABL1 protein expression are needed to achieve more effective therapy. Using a high-content antibody microarray and bioinformatics analyses, we investigated differences in the proteome and phosphorylation landscape of Imatinib (IM)-resistant cells and identified highly activated members of the eukaryotic translation initiation complex (eIF4F), particularly eIF4G1, a core component of eIF4F. These eIF4F complex members are highly expressed and activated in CD34
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Registered trials
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