ArticleProceedings of the National Academy of Sciences of the United States of America2014
Bypass of the pre-60S ribosomal quality control as a pathway to oncogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
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
59 citing papers in PubMed, 79 citations in OpenAlex.
- Ribosome biogenesis and selective translational control as oncogenic vulnerabilities in hematologic malignancies.Molecular cancer · 2026Review
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Systematic analysis of noncanonical ribosomal protein paralogs does not provide evidence for specialized functions inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Proteomics-based characterization of ribosome heterogeneity in adult mouse organs.Cellular and molecular life sciences : CMLS · 2025Article
- Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Review
- Article
- The kinase Rio1 and a ribosome collision-dependent decay pathway survey the integrity of 18S rRNA cleavage.PLoS biology · 2024Article
- Nucleolar stress: Molecular mechanisms and related human diseases.Cancer science · 2023Review
- Quality control ensures fidelity in ribosome assembly and cellular health.The Journal of cell biology · 2023Review
- Using DMS-MaPseq to uncover the roles of DEAD-box proteins in ribosome assembly.Methods (San Diego, Calif.) · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- The chaperone Tsr2 regulates Rps26 release and reincorporation from mature ribosomes to enable a reversible, ribosome-mediated response to stress.Science advances · 2022Article
- Mutational analysis of ribosomal proteins in a cohort of pediatric patients with T-cell acute lymphoblastic leukemia reveals Q123R, a novel mutation in RPL10.Frontiers in genetics · 2022Article
- Small but Mighty-The Emerging Role of snoRNAs in Hematological Malignancies.Non-coding RNA · 2021Review
- Mitochondrial mistranslation modulated by metabolic stress causes cardiovascular disease and reduced lifespan.Aging cell · 2021Article
- Extraribosomal Functions of Cytosolic Ribosomal Proteins in Plants.Frontiers in plant science · 2021Review
- Review
- Structural basis for the transition from translation initiation to elongation by an 80S-eIF5B complex.Nature communications · 2020Article
- Hallmarks of ribosomopathies.Nucleic acids research · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Ribosomopathies are a class of diseases caused by mutations that affect the biosynthesis and/or functionality of the ribosome. Although they initially present as hypoproliferative disorders, such as anemia, patients have elevated risk of hyperproliferative disease (cancer) by midlife. Here, this paradox is explored using the rpL10-R98S (uL16-R98S) mutant yeast model of the most commonly identified ribosomal mutation in acute lymphoblastic T-cell leukemia. This mutation causes a late-stage 60S subunit maturation failure that targets mutant ribosomes for degradation. The resulting deficit in ribosomes causes the hypoproliferative phenotype. This 60S subunit shortage, in turn, exerts pressure on cells to select for suppressors of the ribosome biogenesis defect, allowing them to reestablish normal levels of ribosome production and cell proliferation. However, suppression at this step releases structurally and functionally defective ribosomes into the translationally active pool, and the translational fidelity defects of these mutants culminate in destabilization of selected mRNAs and shortened telomeres. We suggest that in exchange for resolving their short-term ribosome deficits through compensatory trans-acting suppressors, cells are penalized in the long term by changes in gene expression that ultimately undermine cellular homeostasis.
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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.