Evidence map›Paper›PMID 28663564›Full record

ArticleScientific reports2017

No cancer predisposition or increased spontaneous mutation frequencies in NEIL DNA glycosylases-deficient mice.

Veslemøy Rolseth, Luisa Luna, Ann Karin Olsen, Rajikala Suganthan, Katja Scheffler, Christine G Neurauter, Ying Esbensen, Anna Kuśnierczyk, Gunn A Hildrestrand, Anne Graupner and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
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  10. Article
  11. Article
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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

15 authors at 4 institutions in 1 country.

Veslemøy RolsethDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway. vesrol@ous-hf.no.
Luisa LunaDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway. luisa.luna@rr-research.no.
Ann Karin OlsenCentre of Environmental Radioactivity (CERAD CoE), Norway and Department of Molecular Biology, Norwegian Institute of Public Health, Oslo, Norway.ORCID 0000-0003-3982-5213
Rajikala SuganthanDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway.
Katja SchefflerInstitute of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7491, Trondheim, Norway.
Christine G NeurauterDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway.
Ying EsbensenDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Nordbyhagen, 1474, Norway.
Anna KuśnierczykInstitute of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7491, Trondheim, Norway.
Gunn A HildrestrandDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway.
Anne GraupnerCentre of Environmental Radioactivity (CERAD CoE), Norway and Department of Molecular Biology, Norwegian Institute of Public Health, Oslo, Norway.
Jill M AndersenCentre of Environmental Radioactivity (CERAD CoE), Norway and Department of Molecular Biology, Norwegian Institute of Public Health, Oslo, Norway.
Geir SlupphaugInstitute of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7491, Trondheim, Norway.
Arne KlunglandDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway.
Hilde NilsenDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Nordbyhagen, 1474, Norway.ORCID 0000-0003-2115-2663
Magnar BjøråsDepartment of Microbiology, University of Oslo, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway. magnar.bjoras@rr-research.no.
Oslo University Hospital · NONorwegian Institute of Public Health · NONorwegian University of Science and Technology · NOUniversity of Oslo · NO

Funding

Validation of a Rodent Mutagenicity AssayR44ES018017 · NIEHS · LITRON LABORATORIES, LTD. · PI DERTINGER, STEPHEN D · 2010 to 2012
$1.8M
NIEHS NIH HHS R44 ES018017
6 · The paper itself

Abstract

Base excision repair (BER) is a major pathway for removal of DNA base lesions and maintenance of genomic stability, which is essential in cancer prevention. DNA glycosylases recognize and remove specific lesions in the first step of BER. The existence of a number of these enzymes with overlapping substrate specificities has been thought to be the reason why single knock-out models of individual DNA glycosylases are not cancer prone. In this work we have characterized DNA glycosylases NEIL1 and NEIL2 (Neil1

Indexed as

Genetic Predisposition to DiseaseMutationMutation RateAnimalsCell LineDisease Models, AnimalDNA GlycosylasesGenetic Association StudiesGenetic LociHydrogen PeroxideMiceMice, KnockoutMultigene FamilyNeoplasmsPotassium DichromateDNA GlycosylasesHydrogen PeroxidePotassium Dichromate

Identifiers

PMID28663564
PMCPMC5491499
OpenAlexW2648905444

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.