Evidence map›Paper›PMID 33510149›Full record

ArticleNature communications2021

Proliferative polyploid cells give rise to tumors via ploidy reduction.

Tomonori Matsumoto, Leslie Wakefield, Alexander Peters, Myron Peto, Paul Spellman, Markus Grompe

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.6field-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

61 citing papers in PubMed, 86 citations in OpenAlex.

  1. Berberine shows potential in mitigating PMApoptosis : an international journal on programmed cell death · 2026
    Article
  2. Review
  3. Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Tomonori MatsumotoDepartment of Pediatrics, Oregon Health and Science University, Portland, OR, USA. tomomatsumototm@gmail.com.ORCID http://orcid.org/0000-0003-4483-2178
Leslie WakefieldDepartment of Pediatrics, Oregon Health and Science University, Portland, OR, USA.
Alexander PetersDepartment of Pediatrics, Oregon Health and Science University, Portland, OR, USA.
Myron PetoDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, OR, USA.
Paul SpellmanDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, OR, USA.
Markus GrompeDepartment of Pediatrics, Oregon Health and Science University, Portland, OR, USA. grompem@ohsu.edu.ORCID http://orcid.org/0000-0002-6616-4345
Oregon Health & Science University · US

Funding

Treatment of Distal Tyrosine Pathway DisordersR01DK048252 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI GROMPE, MARKUS · 1994 to 2017
$5.5M
Liver Cancer Risk with rAAV Gene TherapyR01CA190144 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI GROMPE, MARKUS, NAUGLER, WILLSCOTT E · 2015 to 2019
$3.0M
NCI NIH HHS R01 CA190144NIDDK NIH HHS R01 DK048252
6 · The paper itself

Abstract

Polyploidy is a hallmark of cancer, and closely related to chromosomal instability involved in cancer progression. Importantly, polyploid cells also exist in some normal tissues. Polyploid hepatocytes proliferate and dynamically reduce their ploidy during liver regeneration. This raises the question whether proliferating polyploids are prone to cancer via chromosome missegregation during mitosis and/or ploidy reduction. Conversely polyploids could be resistant to tumor development due to their redundant genomes. Therefore, the tumor-initiation risk of physiologic polyploidy and ploidy reduction is still unclear. Using in vivo lineage tracing we here show that polyploid hepatocytes readily form liver tumors via frequent ploidy reduction. Polyploid hepatocytes give rise to regenerative nodules with chromosome aberrations, which are enhanced by ploidy reduction. Although polyploidy should theoretically prevent tumor suppressor loss, the high frequency of ploidy reduction negates this protection. Importantly, polyploid hepatocytes that undergo multiple rounds of cell division become predominantly mononucleated and are resistant to ploidy reduction. Our results suggest that ploidy reduction is an early step in the initiation of carcinogenesis from polyploid hepatocytes.

Indexed as

PolyploidyAnimalsCells, CulturedCell Transformation, NeoplasticChromosomal InstabilityHepatocytesHumansLiverLiver NeoplasmsMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicMitosisPloidies

Identifiers

PMID33510149
PMCPMC7843634
OpenAlexW3125877452

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.