Evidence map›Paper›PMID 34873230›Full record

ArticleScientific reports2021

Impact of the APOBEC3A/B deletion polymorphism on risk of ovarian cancer.

Liv B Gansmo, Nigar Sofiyeva, Merete Bjørnslett, Pål Romundstad, Kristian Hveem, Lars Vatten, Anne Dørum, Per E Lønning, Stian Knappskog

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. 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

9 authors at 3 institutions in 1 country.

Liv B GansmoK.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, 5021, Bergen, Norway.
Nigar SofiyevaK.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, 5021, Bergen, Norway.
Merete BjørnslettDepartment of Molecular Oncology, Oslo University Hospital Radium Hospitalet, Oslo, Norway.
Pål RomundstadDepartment of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Kristian HveemK.G. Jebsen Center for Genetic Epidemiology, Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Lars VattenDepartment of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Anne DørumDepartment of Gynecologic Oncology, Oslo University Hospital, Norwegian Radium Hospital, Oslo, Norway.
Per E LønningK.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, 5021, Bergen, Norway.
Stian KnappskogK.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, 5021, Bergen, Norway. stian.knappskog@uib.no.ORCID 0000-0002-4153-1655
Haukeland University Hospital · NONorwegian University of Science and Technology · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A germline 29.5-kb deletion variant removes the 3' end of the APOBEC3A gene and a large part of APOBEC3B, creating a hybrid gene that has been linked to increased APOBEC3 activity and DNA damage in human cancers. We genotyped the APOBEC3A/B deletion in hospital-based samples of 1398 Norwegian epithelial ovarian cancer patients without detected BRCA1/2 germline mutations and compared to 1,918 healthy female controls, to assess the potential cancer risk associated with the deletion. We observed an association between APOBEC3A/B status and reduced risk for ovarian cancer (OR = 0.75; CI = 0.61-0.91; p = 0.003) applying the dominant model. Similar results were found in other models. The association was observed both in non-serous and serous cases (dominant model: OR = 0.69; CI = 0.50-0.95; p = 0.018 and OR = 0.77; CI = 0.62-0.96; p = 0.019, respectively) as well as within high-grade serous cases (dominant model: OR = 0.79; CI = 0.59-1.05). For validation purposes, we mined an available large multinational GWAS-based data set of > 18,000 cases and > 26,000 controls for SNP rs12628403, known to be in linkage disequilibrium with the APOBEC3A/B deletion. We found a non-significant trend for SNP rs12628403 being linked to reduced risk of ovarian cancer in general and similar trends for all subtypes. For clear cell cancers, the risk reduction reached significance (OR = 0.85; CI = 0.69-1.00).

Indexed as

AgedBiomarkers, TumorCase-Control StudiesCytidine DeaminaseFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenotypeGerm-Line MutationHumansMiddle AgedMinor Histocompatibility AntigensOvarian NeoplasmsPolymorphism, GeneticProteinsSequence DeletionAPOBEC3A protein, humanAPOBEC3B protein, humanBiomarkers, TumorCytidine DeaminaseMinor Histocompatibility AntigensProteins

Identifiers

PMID34873230
PMCPMC8648731
OpenAlexW4200447612

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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.