Evidence map›Paper›PMID 26208354›Full record

Trial reportScientific reports2015

Implementation of genome-wide complex trait analysis to quantify the heritability in multiple myeloma.

Jonathan S Mitchell, David C Johnson, Kevin Litchfield, Peter Broderick, Niels Weinhold, Faith E Davies, Walter A Gregory, Graham H Jackson, Martin Kaiser, Gareth J Morgan and 1 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.

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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

11 authors at 4 institutions in 2 countries.

Jonathan S MitchellMolecular and Population Genetics, Division of Genetics and Epidemiology, The Institute of Cancer Research, Surrey, UK.
David C JohnsonDepartment of Haemato-Oncology, Division of Pathology, The Institute of Cancer Research, Surrey, UK.
Kevin LitchfieldMolecular and Population Genetics, Division of Genetics and Epidemiology, The Institute of Cancer Research, Surrey, UK.
Peter BroderickMolecular and Population Genetics, Division of Genetics and Epidemiology, The Institute of Cancer Research, Surrey, UK.
Niels WeinholdMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Faith E DaviesDepartment of Haemato-Oncology, Division of Pathology, The Institute of Cancer Research, Surrey, UK.
Walter A GregoryLeeds Institute of Molecular Medicine, Section of Clinical Trials Research, University of Leeds, Leeds, UK.
Graham H JacksonRoyal Victoria Infirmary, Newcastle upon Tyne, UK.
Martin KaiserCentre for Myeloma Research, Division of Molecular Pathology, The Institute of Cancer Research, Sutton, UK.
Gareth J MorganMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Richard S HoulstonMolecular and Population Genetics, Division of Genetics and Epidemiology, The Institute of Cancer Research, Surrey, UK.
Institute of Cancer Research · GBUniversity of Arkansas for Medical Sciences · USRoyal Victoria Infirmary · GBUniversity of Leeds · GB

Funding

Cancer Research UK 10410Cancer Research UK 14261Cancer Research UK 15116Cancer Research UK 17761Medical Research Council G0100132Wellcome Trust
6 · The paper itself

Abstract

A sizeable fraction of multiple myeloma (MM) is expected to be explained by heritable factors. Genome-wide association studies (GWAS) have successfully identified a number of common single-nucleotide polymorphisms (SNPs) influencing MM risk. While these SNPs only explain a small proportion of the genetic risk it is unclear how much is left to be detected by other, yet to be identified, common SNPs. Therefore, we applied Genome-Wide Complex Trait Analysis (GCTA) to 2,282 cases and 5,197 controls individuals to estimate the heritability of MM. We estimated that the heritability explained by known common MM risk SNPs identified in GWAS was 2.9% (± 2.4%), whereas the heritability explained by all common SNPs was 15.2% (± 2.8%). Comparing the heritability explained by the common variants with that from family studies, a fraction of the heritability may be explained by other genetic variants, such as rare variants. In summary, our results suggest that known MM SNPs only explain a small proportion of the heritability and more common SNPs remain to be identified.

Indexed as

Genetic Predisposition to DiseaseGenome, HumanPolymorphism, Single NucleotideQuantitative Trait, HeritableCase-Control StudiesGenetic VariationGenome-Wide Association StudyHumansModels, GeneticMultiple MyelomaPhenotype

Identifiers

PMID26208354
PMCPMC4513545
OpenAlexW1864715623

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.