Evidence map›Paper›PMID 20128929›Full record

ArticleMolecular cancer2010

Unscheduled expression of CDC25B in S-phase leads to replicative stress and DNA damage.

Béatrix Bugler, Estelle Schmitt, Bernadette Aressy, Bernard Ducommun

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  5. DNA replication stress: oncogenes in the spotlight.Genetics and molecular biology · 2019
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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

4 authors at 3 institutions in 2 countries.

Béatrix BuglerUniversité de Toulouse, LBCMCP, Toulouse, France.
Estelle Schmitt
Bernadette Aressy
Bernard Ducommun
Laboratoire de Biologie Cellulaire et Moléculaire du Contrôle de la Prolifération · FRCentre National de la Recherche Scientifique · FRHôpital Notre-Dame · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCDC25B phosphatase is a cell cycle regulator that plays a critical role in checkpoint control. Up-regulation of CDC25B expression has been documented in a variety of human cancers, however, the relationships with the alteration of the molecular mechanisms that lead to oncogenesis still remain unclear. To address this issue we have investigated, in model cell lines, the consequences of unscheduled and elevated CDC25B levels.

resultsWe report that increased CDC25B expression leads to DNA damage in the absence of genotoxic treatment. H2AX phosphorylation is detected in S-phase cells and requires active replication. We also report that CDC25B expression impairs DNA replication and results in an increased recruitment of the CDC45 replication factor onto chromatin. Finally, we observed chromosomal aberrations that are also enhanced upon CDC25B expression.

conclusionOverall, our results demonstrate that a moderate and unscheduled increase in CDC25B level, as observed in a number of human tumours, is sufficient to overcome the S-phase checkpoint efficiency thus leading to replicative stress and genomic instability.

Indexed as

DNA DamageS PhaseStress, Physiologicalcdc25 PhosphatasesCell Cycle ProteinsCell Line, TumorChromatinChromosomal InstabilityHistonesHumansProtein BindingStaining and LabelingCDC25B protein, humancdc25 PhosphatasesCDC45 protein, humanCell Cycle ProteinsChromatinH2AX protein, humanHistones

Identifiers

PMID20128929
PMCPMC2825247
OpenAlexW2111652738

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.