Evidence map›Paper›PMID 32383162›Full record

ArticleInternational journal of cancer2020

Clustering of known low and moderate risk alleles rather than a novel recessive high-risk gene in non-BRCA1/2 sib trios affected with breast cancer.

Florentine S Hilbers, Peter J van 't Hof, Caro M Meijers, Hailiang Mei, Kyriaki Michailidou, Joe Dennis, Frans B L Hogervorst, Petra M Nederlof, Christi J van Asperen, Peter Devilee

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In one paragraph

Article in International journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Hereditary cancer syndromes.World journal of clinical oncology · 2023
    Review
  2. 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

10 authors at 3 institutions in 3 countries.

Florentine S HilbersDepartment of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands.ORCID 0000-0002-6764-3102
Peter J van 't HofSequence Analysis Support Core, Leiden University Medical Centre, Leiden, The Netherlands.
Caro M MeijersDepartment of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands.
Hailiang MeiSequence Analysis Support Core, Leiden University Medical Centre, Leiden, The Netherlands.
Kyriaki MichailidouCentre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Joe DennisCentre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Frans B L HogervorstDepartment of Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Petra M NederlofDepartment of Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Christi J van AsperenDepartment of Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands.
Peter DevileeDepartment of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands.ORCID 0000-0002-8023-2009
Leiden University · NLThe Netherlands Cancer Institute · NLUniversity of Cambridge · GB

Funding

Cancer Research UK
6 · The paper itself

Abstract

Breast cancer risk is approximately twice as high in first-degree relatives of female breast cancer cases than in women in the general population. Less than half of this risk can be attributed to the currently known genetic risk factors. Recessive risk alleles represent a relatively underexplored explanation for the remainder of familial risk. To address this, we selected 19 non-BRCA1/2 breast cancer families in which at least three siblings were affected, while no first-degree relatives of the previous or following generation had breast cancer. Germline DNA from one of the siblings was subjected to exome sequencing, while all affected siblings were genotyped using SNP arrays to assess haplotype sharing and to calculate a polygenic risk score (PRS) based on 160 low-risk variants. We found no convincing candidate recessive alleles among exome sequencing variants in genomic regions for which all three siblings shared two haplotypes. However, we found two families in which all affected siblings carried the CHEK2*1100delC. In addition, the average normalized PRS of the "recessive" family probands (0.81) was significantly higher than that in both general population cases (0.35, P = .026) and controls (P = .0004). These findings suggest that the familial aggregation is, at least in part, explained by a polygenic effect of common low-risk variants and rarer intermediate-risk variants, while we did not find evidence of a role for novel recessive risk alleles.

Indexed as

Polymorphism, Single NucleotideBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsCase-Control StudiesCheckpoint Kinase 2Exome SequencingFemaleGenetic Predisposition to DiseaseGerm-Line MutationHaplotypesHigh-Throughput Nucleotide SequencingHumansMultifactorial InheritancePedigreeSiblingsBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanCheckpoint Kinase 2CHEK2 protein, humanbreast cancerexomepolygenicrecessivesusceptibility

Identifiers

PMID32383162
PMCPMC7540545
OpenAlexW3021057917

What OpenQuestion holds

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LicenceCC BY
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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.