Evidence map›Paper›PMID 34462428›Full record

ReviewSignal transduction and targeted therapy2021

Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy.

Jian Kang, Natalie Brajanovski, Keefe T Chan, Jiachen Xuan, Richard B Pearson, Elaine Sanij

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed
20.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

253 citing papers in PubMed, 391 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  7. iScience · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Inherited human TFIIIA deficiency disrupts T cell development.medRxiv : the preprint server for health sciences · 2026
    Article
  16. Article
  17. RiboScreenBiomedicines · 2026
    Review
  18. Article
  19. Article
  20. Science advances · 2026
    Article

193 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Jian Kang *Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Natalie Brajanovski *Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Keefe T ChanDivision of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Jiachen XuanDivision of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Richard B PearsonDivision of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Elaine SanijDivision of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia. esanij@svi.edu.au.
Peter MacCallum Cancer Centre · AUMonash University · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ribosome biogenesis and protein synthesis are fundamental rate-limiting steps for cell growth and proliferation. The ribosomal proteins (RPs), comprising the structural parts of the ribosome, are essential for ribosome assembly and function. In addition to their canonical ribosomal functions, multiple RPs have extra-ribosomal functions including activation of p53-dependent or p53-independent pathways in response to stress, resulting in cell cycle arrest and apoptosis. Defects in ribosome biogenesis, translation, and the functions of individual RPs, including mutations in RPs have been linked to a diverse range of human congenital disorders termed ribosomopathies. Ribosomopathies are characterized by tissue-specific phenotypic abnormalities and higher cancer risk later in life. Recent discoveries of somatic mutations in RPs in multiple tumor types reinforce the connections between ribosomal defects and cancer. In this article, we review the most recent advances in understanding the molecular consequences of RP mutations and ribosomal defects in ribosomopathies and cancer. We particularly discuss the molecular basis of the transition from hypo- to hyper-proliferation in ribosomopathies with elevated cancer risk, a paradox termed "Dameshek's riddle." Furthermore, we review the current treatments for ribosomopathies and prospective therapies targeting ribosomal defects. We also highlight recent advances in ribosome stress-based cancer therapeutics. Importantly, insights into the mechanisms of resistance to therapies targeting ribosome biogenesis bring new perspectives into the molecular basis of cancer susceptibility in ribosomopathies and new clinical implications for cancer therapy.

Indexed as

Molecular Targeted TherapyCell Cycle CheckpointsCell ProliferationGenetic Diseases, InbornHumansMutationNeoplasmsRibosomal ProteinsRibosomesRibosomal Proteins

Identifiers

PMID34462428
PMCPMC8405630
OpenAlexW3198338615

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.