Evidence map›Paper›PMID 26010955›Full record

ReviewGenes2015

Replication stress in Mammalian cells and its consequences for mitosis.

Camille Gelot, Indiana Magdalou, Bernard S Lopez

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.9field-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

75 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The landscape of structural variation in pediatric cancer.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. ISG15: A link between innate immune signaling, DNA replication, and genome stability.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
  20. Article

15 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 1 country.

Camille GelotInstitut de Cancérologie Gustave Roussy, CNRS UMR 8200 and Université Paris Sud, Equipe labélisée "LIGUE 2014", 114, Rue Edouard Vaillant, 94805 Villejuif, France. camille.gelot@gustaveroussy.fr.
Indiana MagdalouInstitut de Cancérologie Gustave Roussy, CNRS UMR 8200 and Université Paris Sud, Equipe labélisée "LIGUE 2014", 114, Rue Edouard Vaillant, 94805 Villejuif, France. indiana.magdalou@gustaveroussy.fr.
Bernard S LopezInstitut de Cancérologie Gustave Roussy, CNRS UMR 8200 and Université Paris Sud, Equipe labélisée "LIGUE 2014", 114, Rue Edouard Vaillant, 94805 Villejuif, France. bernard.lopez@gustaveroussy.fr.
Centre National de la Recherche Scientifique · FRInstitut Gustave Roussy · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The faithful transmission of genetic information to daughter cells is central to maintaining genomic stability and relies on the accurate and complete duplication of genetic material during each cell cycle. However, the genome is routinely exposed to endogenous and exogenous stresses that can impede the progression of replication. Such replication stress can be an early cause of cancer or initiate senescence. Replication stress, which primarily occurs during S phase, results in consequences during mitosis, jeopardizing chromosome segregation and, in turn, genomic stability. The traces of replication stress can be detected in the daughter cells during G1 phase. Alterations in mitosis occur in two types: 1) local alterations that correspond to breaks, rearrangements, intertwined DNA molecules or non-separated sister chromatids that are confined to the region of the replication dysfunction; 2) genome-wide chromosome segregation resulting from centrosome amplification (although centrosomes do not contain DNA), which amplifies the local replication stress to the entire genome. Here, we discuss the endogenous causes of replication perturbations, the mechanisms of replication fork restart and the consequences for mitosis, chromosome segregation and genomic stability.

Indexed as

anaphase bridgescentrosomefragile siteshomologous recombinationmicronucleimitosisreplication stresssingle-ended DSB

Identifiers

PMID26010955
PMCPMC4488665
OpenAlexW1575623650

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.