Evidence map›Paper›PMID 29754823›Full record

ArticleMolecular cell2018

Polε Instability Drives Replication Stress, Abnormal Development, and Tumorigenesis.

Roberto Bellelli, Valerie Borel, Clare Logan, Jennifer Svendsen, Danielle E Cox, Emma Nye, Kay Metcalfe, Susan M O'Connell, Gordon Stamp, Helen R Flynn and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
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  3. Functional Characterization ofDiseases (Basel, Switzerland) · 2026
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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

14 authors at 5 institutions in 2 countries.

Roberto BellelliThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Valerie BorelThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Clare LoganMRC Institute of Genetics & Molecular Medicine, The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK.
Jennifer SvendsenThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Danielle E CoxThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Emma NyeThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Kay MetcalfeDepartment of Genetic Medicine, St Mary's Hospital, Oxford Road, Manchester, M13 OJH, UK.
Susan M O'ConnellDepartment of Paediatrics, Cork University Hospital, Wilton, Cork T12 DC4A, Ireland.
Gordon StampThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Helen R FlynnThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Ambrosius P SnijdersThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
François LassaillyThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Andrew JacksonMRC Institute of Genetics & Molecular Medicine, The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK.
Simon J BoultonThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK. Electronic address: simon.boulton@crick.ac.uk.
The Francis Crick Institute · GBCork University Hospital · IEMRC Institute of Genetics and Molecular Medicine · GBSt Mary's Hospital · GBUniversity of Edinburgh · GB

Funding

Cancer Research UK FC0010048Medical Research Council FC0010048Medical Research Council MC_PC_U127580972Medical Research Council MC_UU_00007/5Wellcome TrustWellcome Trust 104558/Z/14/ZWellcome Trust FC0010048
6 · The paper itself

Abstract

DNA polymerase ε (POLE) is a four-subunit complex and the major leading strand polymerase in eukaryotes. Budding yeast orthologs of POLE3 and POLE4 promote Polε processivity in vitro but are dispensable for viability in vivo. Here, we report that POLE4 deficiency in mice destabilizes the entire Polε complex, leading to embryonic lethality in inbred strains and extensive developmental abnormalities, leukopenia, and tumor predisposition in outbred strains. Comparable phenotypes of growth retardation and immunodeficiency are also observed in human patients harboring destabilizing mutations in POLE1. In both Pole4

Indexed as

DNA ReplicationAnimalsCarcinogenesisCells, CulturedDevelopmental DisabilitiesDNA Polymerase IIEmbryo, MammalianFemaleGrowth DisordersHumansInfant, NewbornLeukopeniaMaleMiceMice, Inbred C57BLMice, KnockoutDNA Polymerase IITumor Suppressor Protein p53DNA polymerase εDNA replicationgenome stabilityp53POLE1/2 mutationstumorigenesis

Identifiers

PMID29754823
PMCPMC5972231
OpenAlexW2800442359

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.