Evidence map›Paper›PMID 25575543›Full record

ArticleBlood2015

Ribosomopathies and the paradox of cellular hypo- to hyperproliferation.

Kim De Keersmaecker, Sergey O Sulima, Jonathan D Dinman

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

81 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Science advances · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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 · 2025
    Article
  12. Review
  13. 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 · 2025
    Review
  14. Ribosomes: from conserved origin to functional/medical mobility and heterogeneity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  15. Impacts of ribosomal RNA sequence variation on gene expression and phenotype.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  16. Ribosomal protein paralogues in ribosome specialization.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Article

21 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

3 authors at 3 institutions in 2 countries.

Kim De KeersmaeckerKU Leuven Department of Oncology, Leuven, Belgium; VIB Center for the Biology of Disease, Leuven, Belgium; and.
Sergey O SulimaKU Leuven Department of Oncology, Leuven, Belgium; VIB Center for the Biology of Disease, Leuven, Belgium; and.
Jonathan D DinmanDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD.
KU Leuven · BEUniversity of Maryland, College Park · USVIB-KU Leuven Center for Cancer Biology · BE

Funding

X-linked Dyskeratosis Congenita and Ribosomal FrameshiftingR01HL119439 · NHLBI · UNIV OF MARYLAND, COLLEGE PARK · PI DINMAN, JONATHAN D, RUGGERO, DAVIDE · 2014 to 2017
$2.8M
Training Program in Cell & Molecular BiologyT32GM080201 · NIGMS · UNIV OF MARYLAND, COLLEGE PARK · PI DELWICHE, CHARLES F · 2009 to 2019
$1.6M
European Research Council 334946NHLBI NIH HHS R01 HL119438NHLBI NIH HHS R01 HL119439NIGMS NIH HHS T32 GM080201
6 · The paper itself

Abstract

Ribosomopathies are largely congenital diseases linked to defects in ribosomal proteins or biogenesis factors. Some of these disorders are characterized by hypoproliferative phenotypes such as bone marrow failure and anemia early in life, followed by elevated cancer risks later in life. This transition from hypo- to hyperproliferation presents an intriguing paradox in the field of hematology known as "Dameshek's riddle." Recent cancer sequencing studies also revealed somatically acquired mutations and deletions in ribosomal proteins in T-cell acute lymphoblastic leukemia and solid tumors, further extending the list of ribosomopathies and strengthening the association between ribosomal defects and oncogenesis. In this perspective, we summarize and comment on recent findings in the field of ribosomopathies. We explain how ribosomopathies may provide clues to help explain Dameshek's paradox and highlight some of the open questions and challenges in the field.

Indexed as

AnimalsCell ProliferationHumansNeoplasmsRibosomal ProteinsRibosomesRibosomal Proteins

Identifiers

PMID25575543
PMCPMC4342353
OpenAlexW2071172473

What OpenQuestion holds

Textmetadata
LicenceTDM
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.