Evidence map›Paper›PMID 33087841›Full record

ArticleCommunications biology2020

Cep55 overexpression promotes genomic instability and tumorigenesis in mice.

Debottam Sinha, Purba Nag, Devathri Nanayakkara, Pascal H G Duijf, Andrew Burgess, Prahlad Raninga, Veronique A J Smits, Amanda L Bain, Goutham Subramanian, Meaghan Wall and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 59 citations in OpenAlex.

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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

13 authors at 7 institutions in 2 countries.

Debottam SinhaQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.
Purba NagQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.ORCID 0000-0002-6863-5438
Devathri NanayakkaraQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.
Pascal H G DuijfUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, 4102, QLD, Australia.ORCID 0000-0001-8646-9843
Andrew BurgessANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID 0000-0003-4536-9226
Prahlad RaningaQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.
Veronique A J SmitsUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Amanda L BainQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.
Goutham SubramanianQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia.ORCID 0000-0002-2835-8464
Meaghan WallVictorian Cancer Cytogenetics Service, St. Vincent's Hospital, Fitzroy, Melbourne, Australia.
John W FinnieDiscipline of Anatomy and Pathology, Adelaide Medical School, University of Adelaide and SA Pathology, Adelaide, Australia.
Murugan KalimuthoQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia. Murugan.Kalimutho@qimrberghofer.edu.au.ORCID 0000-0002-0772-8673
Kum Kum KhannaQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006, QLD, Australia. KumKum.Khanna@qimrberghofer.edu.au.
QIMR Berghofer Medical Research Institute · AUGriffith University · AUSouth Australia Pathology · AUSt Vincent's Hospital Melbourne · AUThe University of Sydney · AUTranslational Research Institute · AUUniversidad de La Laguna · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High expression of centrosomal protein CEP55 has been correlated with clinico-pathological parameters across multiple human cancers. Despite significant in vitro studies and association of aberrantly overexpressed CEP55 with worse prognosis, its causal role in vivo tumorigenesis remains elusive. Here, using a ubiquitously overexpressing transgenic mouse model, we show that Cep55 overexpression causes spontaneous tumorigenesis and accelerates Trp53

Indexed as

Gene ExpressionGenomic InstabilityAnimalsBiomarkers, TumorBiopsyCell Cycle ProteinsCell LineCell Transformation, NeoplasticCheckpoint Kinase 1Disease SusceptibilityFibroblastsGenotypeImmunohistochemistryKaryotypeLymph NodesMiceBiomarkers, TumorCell Cycle ProteinsCep55 protein, mouseCheckpoint Kinase 1Chek1 protein, mouseProto-Oncogene Proteins c-aktTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID33087841
PMCPMC7578791
OpenAlexW3093509760

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.