Evidence map›Paper›PMID 25741376›Full record

ArticleCell division2015

Cyclin E2 is the predominant E-cyclin associated with NPAT in breast cancer cells.

Samuel Rogers, Brian S Gloss, Christine S Lee, Claudio Marcelo Sergio, Marcel E Dinger, Elizabeth A Musgrove, Andrew Burgess, Catherine Elizabeth Caldon

Open access · goldAbstract read
In one paragraph

Article in Cell division, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  9. The Rad53Nature communications · 2020
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  15. Review
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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

8 authors at 5 institutions in 2 countries.

Samuel RogersThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia.
Brian S GlossThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia ; St Vincent's Clinical School, Faculty of Medicine UNSW, Sydney, Australia.
Christine S LeeThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia.
Claudio Marcelo SergioThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia.
Marcel E DingerThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia ; St Vincent's Clinical School, Faculty of Medicine UNSW, Sydney, Australia.
Elizabeth A MusgroveWolfson Wohl Cancer Research Centre, University of Glasgow, Garscube Estate, Glasgow, G61 1QH UK.
Andrew BurgessThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia ; St Vincent's Clinical School, Faculty of Medicine UNSW, Sydney, Australia.
Catherine Elizabeth CaldonThe Kinghorn Cancer Centre and Cancer Research Program, Garvan Institute of Medical Research, Sydney, NSW Australia ; St Vincent's Clinical School, Faculty of Medicine UNSW, Sydney, Australia.
Garvan Institute of Medical Research · AUSt Vincent's Clinic · AUThe Kinghorn Cancer Centre · AUUniversity of Glasgow · GBUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cyclin E oncogene activates CDK2 to drive cells from G1 to S phase of the cell cycle to commence DNA replication. It coordinates essential cellular functions with the cell cycle including histone biogenesis, splicing, centrosome duplication and origin firing for DNA replication. The two E-cyclins, E1 and E2, are assumed to act interchangeably in these functions. However recent reports have identified unique functions for cyclins E1 and E2 in different tissues, and particularly in breast cancer.

findingsCyclins E1 and E2 localise to distinct foci in breast cancer cells as well as co-localising within the cell. Both E-cyclins are found in complex with CDK2, at centrosomes and with the splicing machinery in nuclear speckles. However cyclin E2 uniquely co-localises with NPAT, the main activator of cell-cycle regulated histone transcription. Increased cyclin E2, but not cyclin E1, expression is associated with high expression of replication-dependent histones in breast cancers.

conclusionsThe preferential localisation of cyclin E1 or cyclin E2 to distinct foci indicates that each E-cyclin has unique roles. Cyclin E2 uniquely interacts with NPAT in breast cancer cells, and is associated with higher levels of histones in breast cancer. This could explain the unique correlations of high cyclin E2 expression with poor outcome and genomic instability in breast cancer.

Indexed as

Breast cancerCajal bodiesCDK2CentrosomeCyclin E1Cyclin E2Histone Locus bodies (HLB)HistonesNPATSpliceosomes

Identifiers

PMID25741376
PMCPMC4349318
OpenAlexW2131149703

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.