ArticleHemaSphere2026
A RiboCancer cell line panel reveals that CLL-associated Rps15 mutations translationally rewire transcription through codon-specific tRNA accommodation defects.
Article in HemaSphere, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
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Authors and funding
27 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent point mutations in ribosomal proteins (RPs) RPL10 and RPS15 are found in T-cell acute lymphoblastic leukemia (T-ALL) and chronic lymphocytic leukemia (CLL), respectively. Furthermore, deletions of RPL5, RPL11, and RPL22 are frequent in hematologic diseases such as Diamond Blackfan Anemia, T-ALL, multiple myeloma, and in a variety of solid tumors. Yet, the role of these RP defects in dysregulation of the ribosomal translation function remains poorly understood. We engineered an isogenic RiboCancer cell line library modeling the most recurrent RP defects in blood and solid cancers and characterized it by a multi-omics translatome analysis (proteome, Ribo-seq, and total RNA-seq) as well as RiboMethSeq. Within this RiboCancer panel, CLL
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Registered trials
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