Evidence map›Paper›PMID 28880866›Full record

ArticlePLoS genetics2017

Ribosomal DNA copy number amplification and loss in human cancers is linked to tumor genetic context, nucleolus activity, and proliferation.

Meng Wang, Bernardo Lemos

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
5.8field-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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. A complete human pancreatic cancer genome.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Mechanisms of ribosomopathy and phase separation-related ribosomopathy.Journal of Zhejiang University. Science. B · 2025
    Review
  11. Assessing Human Ribosomal DNA Variation and Its Association With Phenotypic Outcomes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

19 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

2 authors.

Meng WangDepartment of Environmental Health & Molecular and Integrative Physiological Sciences program, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, United States of America.ORCID http://orcid.org/0000-0003-3209-1026
Bernardo LemosDepartment of Environmental Health & Molecular and Integrative Physiological Sciences program, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, United States of America.ORCID http://orcid.org/0000-0001-6996-9483

Funding

Novel markers of exposure and pathways of response to ChromiumR01ES027981 · NIEHS · UNIVERSITY OF ARIZONA · PI LEMOS, BERNARDO · 2018 to 2022
$2.0M
NIEHS NIH HHS R01 ES027981
6 · The paper itself

Abstract

Ribosomal RNAs (rRNAs) are transcribed from two multicopy DNA arrays: the 5S ribosomal DNA (rDNA) array residing in a single human autosome and the 45S rDNA array residing in five human autosomes. The arrays are among the most variable segments of the genome, exhibit concerted copy number variation (cCNV), encode essential components of the ribosome, and modulate global gene expression. Here we combined whole genome data from >700 tumors and paired normal tissues to provide a portrait of rDNA variation in human tissues and cancers of diverse mutational signatures, including stomach and lung adenocarcinomas, ovarian cancers, and others of the TCGA panel. We show that cancers undergo coupled 5S rDNA array expansion and 45S rDNA loss that is accompanied by increased estimates of proliferation rate and nucleolar activity. These somatic changes in rDNA CN occur in a background of over 10-fold naturally occurring rDNA CN variation across individuals and cCNV of 5S-45S arrays in some but not all tissues. Analysis of genetic context revealed associations between cancer rDNA CN amplification or loss and the presence of specific somatic alterations, including somatic SNPs and copy number gain/losses in protein coding genes across the cancer genome. For instance, somatic inactivation of the tumor suppressor gene TP53 emerged with a strong association with coupled 5S expansion / 45S loss in several cancers. Our results uncover frequent and contrasting changes in the 5S and 45S rDNA along rapidly proliferating cell lineages with high nucleolar activity. We suggest that 5S rDNA amplification facilitates increased proliferation, nucleolar activity, and ribosomal synthesis in cancer, whereas 45S rDNA loss emerges as a byproduct of transcription-replication conflict in rapidly replicating tumor cells. The observations raise the prospects of using the rDNA arrays as re-emerging targets for the design of novel strategies in cancer therapy.

Indexed as

Cell NucleolusCell ProliferationDNA Copy Number VariationsDNA, RibosomalGenome, HumanHumansIn Situ Hybridization, FluorescenceNeoplasmsPolymorphism, Single NucleotideRNA, RibosomalRNA, Ribosomal, 5SDNA, RibosomalRNA, RibosomalRNA, ribosomal, 45SRNA, Ribosomal, 5S

Identifiers

PMID28880866
PMCPMC5605086
OpenAlexW2752006971

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.