Evidence map›Paper›PMID 30854481›Full record

ArticleCommunications biology2019

Genome-wide interaction and pathway-based identification of key regulators in multiple myeloma.

Subhayan Chattopadhyay, Hauke Thomsen, Pankaj Yadav, Miguel Inacio da Silva Filho, Niels Weinhold, Markus M Nöthen, Per Hoffman, Uta Bertsch, Stefanie Huhn, Gareth J Morgan and 4 more

Abstract read
In one paragraph

Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. TargetingPathology oncology research : POR · 2021
    Article
  8. Article
  9. Article
  10. 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

14 authors.

Subhayan ChattopadhyayDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-8599-2971
Hauke ThomsenDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany.
Pankaj YadavDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany.
Miguel Inacio da Silva FilhoDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany.
Niels WeinholdUniversity Clinic Heidelberg, Internal Medicine V, Heidelberg, 69117, Germany.
Markus M NöthenInstitute of Human Genetics, University of Bonn, Bonn, 53127, Germany.
Per HoffmanInstitute of Human Genetics, University of Bonn, Bonn, 53127, Germany.
Uta BertschUniversity Clinic Heidelberg, Internal Medicine V, Heidelberg, 69117, Germany.
Stefanie HuhnUniversity Clinic Heidelberg, Internal Medicine V, Heidelberg, 69117, Germany.
Gareth J MorganMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, 72205, AR, USA.
Hartmut GoldschmidtUniversity Clinic Heidelberg, Internal Medicine V, Heidelberg, 69117, Germany.
Richard HoulstonDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, SW7 3RP, UK.ORCID http://orcid.org/0000-0002-5268-0242
Kari HemminkiDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany.
Asta FörstiDivision of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, 69120, Germany. A.Foersti@dkfz.de.

Funding

Cancer Research UK C1298/A8362Wellcome Trust
6 · The paper itself

Abstract

Inherited genetic susceptibility to multiple myeloma has been investigated in a number of studies. Although 23 individual risk loci have been identified, much of the genetic heritability remains unknown. Here we carried out genome-wide interaction analyses on two European cohorts accounting for 3,999 cases and 7,266 controls and characterized genetic susceptibility to multiple myeloma with subsequent meta-analysis that discovered 16 unique interacting loci. These risk loci along with previously known variants explain 17% of the heritability in liability scale. The genes associated with the interacting loci were found to be enriched in transforming growth factor beta signaling and circadian rhythm regulation pathways suggesting immunoglobulin trait modulation, T

Indexed as

Disease SusceptibilityGenome-Wide Association StudySignal TransductionChromosome MappingGene Regulatory NetworksGenetic LociGenetic Predisposition to DiseaseHumansMultiple MyelomaPolymorphism, Single Nucleotide

Identifiers

PMID30854481
PMCPMC6399257

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.