Evidence map›Paper›PMID 26876972›Full record

ArticleNature communications2016

The presence of extra chromosomes leads to genomic instability.

Verena Passerini, Efrat Ozeri-Galai, Mirjam S de Pagter, Neysan Donnelly, Sarah Schmalbrock, Wigard P Kloosterman, Batsheva Kerem, Zuzana Storchová

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
16.2field-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

180 citing papers in PubMed, 304 citations in OpenAlex.

  1. Dna aneuploidy and urothelial carcinoma: A meta-analysis.Current therapeutic research, clinical and experimental · 2026
    Review
  2. Review
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  4. Pretreatment Chromosomal Instability Correlates With Radiation Sensitivity in Squamous Cell Cancers.International journal of radiation oncology, biology, physics · 2026
    Article
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  13. PARP1 Suppression Drives ROS Resistance in Aneuploid Cancer Cells.bioRxiv : the preprint server for biology · 2026
    Article
  14. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
    Review
  15. Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026
    Review
  16. How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026
    Review
  17. Article
  18. Review
  19. Review
  20. Article

120 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

8 authors at 4 institutions in 2 countries.

Verena PasseriniMax Planck Institute of Biochemistry, Am Klopferspitz 18, Martinsried 82152, Germany.
Efrat Ozeri-GalaiDepartment of Genetics, The Alexander Silberman Institute of Life Sciences, Edmond J. Safra Campus, Givat-Ram, Jerusalem 91904, Israel.
Mirjam S de PagterDepartment of Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Universiteitsweg 100, Utrecht 3584 CG, The Netherlands.
Neysan DonnellyMax Planck Institute of Biochemistry, Am Klopferspitz 18, Martinsried 82152, Germany.
Sarah SchmalbrockMax Planck Institute of Biochemistry, Am Klopferspitz 18, Martinsried 82152, Germany.
Wigard P KloostermanDepartment of Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Universiteitsweg 100, Utrecht 3584 CG, The Netherlands.
Batsheva KeremDepartment of Genetics, The Alexander Silberman Institute of Life Sciences, Edmond J. Safra Campus, Givat-Ram, Jerusalem 91904, Israel.
Zuzana StorchováMax Planck Institute of Biochemistry, Am Klopferspitz 18, Martinsried 82152, Germany.
Max Planck Institute of Biochemistry · DEUtrecht University · NLCenter for Integrated Protein Science Munich · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aneuploidy is a hallmark of cancer and underlies genetic disorders characterized by severe developmental defects, yet the molecular mechanisms explaining its effects on cellular physiology remain elusive. Here we show, using a series of human cells with defined aneuploid karyotypes, that gain of a single chromosome increases genomic instability. Next-generation sequencing and SNP-array analysis reveal accumulation of chromosomal rearrangements in aneuploids, with break point junction patterns suggestive of replication defects. Trisomic and tetrasomic cells also show increased DNA damage and sensitivity to replication stress. Strikingly, we find that aneuploidy-induced genomic instability can be explained by the reduced expression of the replicative helicase MCM2-7. Accordingly, restoring near-wild-type levels of chromatin-bound MCM helicase partly rescues the genomic instability phenotypes. Thus, gain of chromosomes triggers replication stress, thereby promoting genomic instability and possibly contributing to tumorigenesis.

Indexed as

AneuploidyCell CycleCell LineChromosomes, Human, Pair 21Chromosomes, Human, Pair 3Chromosomes, Human, Pair 5Chromosomes, Human, Pair 8Comparative Genomic HybridizationDNAFluorescent Antibody TechniqueGenomic InstabilityHCT116 CellsHigh-Throughput Nucleotide SequencingHumansMetaphaseMicroscopy, ConfocalDNAMinichromosome Maintenance Proteins

Identifiers

PMID26876972
PMCPMC4756715
OpenAlexW2352719856

What OpenQuestion holds

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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.