Evidence map›Paper›PMID 27936167›Full record

ArticlePloS one2016

The Slavic NBN Founder Mutation: A Role for Reproductive Fitness?

Eva Seemanova, Raymonda Varon, Jan Vejvalka, Petr Jarolim, Pavel Seeman, Krystyna H Chrzanowska, Martin Digweed, Igor Resnick, Ivo Kremensky, Kathrin Saar and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-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

14 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Journal of clinical medicine · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Importance of Germline and Somatic Alterations in HumanInternational journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Chromosome instability syndromes.Nature reviews. Disease primers · 2019
    Review
  13. Review
  14. Article
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

21 authors at 15 institutions in 9 countries.

Eva SeemanovaDepartment of Clinical Genetics, Institute of Biology and Medical Genetics, 2nd Medical School, Charles University, Prague, Czech Republic.
Raymonda VaronInstitute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Germany.
Jan VejvalkaDepartment of Informatics, 2nd Medical School, Charles University, Prague, Czech Republic.
Petr JarolimDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.ORCID http://orcid.org/0000-0002-9612-8652
Pavel SeemanDNA Laboratory, Department of Pediatric Neurology, 2nd Medical School, Charles University and University Hospital Motol, Prague, Czech Republic.
Krystyna H ChrzanowskaDepartment of Medical Genetics, The Children's Memorial Health Institute, Warsaw, Poland.
Martin DigweedInstitute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Germany.
Igor ResnickDepartment of Bone Marrow Transplantation and Cancer Immunotherapy, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Ivo KremenskyNational Genetics Laboratory, University Hospital of Obstetrics and Gynecology, Medical University, Sofia, Bulgaria.
Kathrin SaarMax Delbrück Center for Molecular Medicine (MDC), Berlin-Buch, Germany.
Katrin HoffmannInstitute of Human Genetics, Martin-Luther University Halle-Wittenberg, Halle, Germany.
Véronique DutrannoyInstitute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Germany.
Mohsen KarbasiyanInstitute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Germany.
Mehdi GhaniTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada.
Ivo BarićDepartment of Paediatrics, University Hospital Center Zagreb and University of Zagreb, School of Medicine, Zagreb, Croatia.
Mustafa TekinDivision of Pediatric Molecular Genetics, Ankara University School of Medicine, Ankara, Turkey.
Peter KovacsLeipzig University Medical Center, IFB AdiposityDiseases, Leipzig, Germany.
Michael KrawczakInstitute of Medical Informatics and Statistics, Christian-Albrechts University, Kiel, Germany.
André ReisInstitute of Human Genetics, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany.
Karl SperlingInstitute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Germany.
Michael NothnagelCologne Center for Genomics, University of Cologne, Köln, Germany.ORCID http://orcid.org/0000-0001-8305-7114
Charité - Universitätsmedizin Berlin · DECharles University · CZAnkara University · TRBrigham and Women's Hospital · USChildren's Memorial Health Institute · PLChristian-Albrechts-Universität zu Kiel · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHadassah Medical Center · ILIFB Adiposity Diseases · DEMartin Luther University Halle-Wittenberg · DEMax Delbrück Center · DEMedical University of Sofia · BGUniversity Hospital Centre Zagreb · HRUniversity of Cologne · DEUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vast majority of patients with Nijmegen Breakage Syndrome (NBS) are of Slavic origin and carry a deleterious deletion (c.657del5; rs587776650) in the NBN gene on chromosome 8q21. This mutation is essentially confined to Slavic populations and may thus be considered a Slavic founder mutation. Notably, not a single parenthood of a homozygous c.657del5 carrier has been reported to date, while heterozygous carriers do reproduce but have an increased cancer risk. These observations seem to conflict with the considerable carrier frequency of c.657del5 of 0.5% to 1% as observed in different Slavic populations because deleterious mutations would be eliminated quite rapidly by purifying selection. Therefore, we propose that heterozygous c.657del5 carriers have increased reproductive success, i.e., that the mutation confers heterozygote advantage. In fact, in our cohort study of the reproductive history of 24 NBS pedigrees from the Czech Republic, we observed that female carriers gave birth to more children on average than female non-carriers, while no such reproductive differences were observed for males. We also estimate that c.657del5 likely occurred less than 300 generations ago, thus supporting the view that the original mutation predated the historic split and subsequent spread of the 'Slavic people'. We surmise that the higher fertility of female c.657del5 carriers reflects a lower miscarriage rate in these women, thereby reflecting the role of the NBN gene product, nibrin, in the repair of DNA double strand breaks and their processing in immune gene rearrangements, telomere maintenance, and meiotic recombination, akin to the previously described role of the DNA repair genes BRCA1 and BRCA2.

Indexed as

Founder EffectMutationAdultCell Cycle ProteinsCohort StudiesCzech RepublicDNA DamageDNA RepairFemaleGenetic Carrier ScreeningHaplotypesHumansMaleMiddle AgedNijmegen Breakage SyndromeNuclear ProteinsCell Cycle ProteinsNBN protein, humanNuclear Proteins

Identifiers

PMID27936167
PMCPMC5148078
OpenAlexW2560340562

What OpenQuestion holds

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Registered trials

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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.