Evidence map›Paper›PMID 36762786›Full record

ReviewCancer science2023

Nucleolar stress: Molecular mechanisms and related human diseases.

Tomohiko Maehama, Miki Nishio, Junji Otani, Tak Wah Mak, Akira Suzuki

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 41 citations in OpenAlex.

  1. ZmDLR9 is required for lateral root development via pre-rRNA processing in maize.The Plant journal : for cell and molecular biology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Deciphering the impact ofGenes & diseases · 2026
    Article
  7. Article
  8. RiboScreenBiomedicines · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Peroxiredoxin 1 safeguards the nucleolar genome from oxidative damage.bioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  20. Review
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

5 authors at 2 institutions in 3 countries.

Tomohiko MaehamaDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID https://orcid.org/0000-0002-9685-2317
Miki NishioDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
Junji OtaniDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
Tak Wah MakPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Akira SuzukiDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID https://orcid.org/0000-0002-5950-8808
Kobe University · JPUniversity Health Network · CA

Funding

Japan Agency for Medical Research and Development 22ama221117h0001Japan Society for the Promotion of Science 20H04905Japan Society for the Promotion of Science 21H04806Project Mirai Cancer Research GrantsTokyo Medical and Dental University Nanken-Kyoten
6 · The paper itself

Abstract

Ribosome biogenesis in the nucleolus is an important process that consumes 80% of a cell's intracellular energy supply. Disruption of this process results in nucleolar stress, triggering the activation of molecular systems that respond to this stress to maintain homeostasis. Although nucleolar stress was originally thought to be caused solely by abnormalities of ribosomal RNA (rRNA) and ribosomal proteins (RPs), an accumulating body of more current evidence suggests that many other factors, including the DNA damage response and oncogenic stress, are also involved in nucleolar stress response signaling. Cells reacting to nucleolar stress undergo cell cycle arrest or programmed death, mainly driven by activation of the tumor suppressor p53. This observation has nominated nucleolar stress as a promising target for cancer therapy. However, paradoxically, some RP mutations have also been implicated in cancer initiation and progression, necessitating caution. In this article, we summarize recent findings on the molecular mechanisms of nucleolar stress and the human ribosomal diseases and cancers that arise in its wake.

Indexed as

NeoplasmsRibosomal ProteinsCell Cycle CheckpointsHumansRibosomesRNA, RibosomalTumor Suppressor Protein p53Ribosomal ProteinsRNA, RibosomalTumor Suppressor Protein p53nucleolar stressp53PICT1ribosomal diseaseRPL11signal transduction

Identifiers

PMID36762786
PMCPMC10154868
OpenAlexW4319812277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.