Heritability estimates on Hodgkin's lymphoma: a genomic- versus population-based approach.

Authors:
Hauke Thomsen, Dr.
Hauke Thomsen, Dr.
GeneWerk GmbH
Senior Bioinformatician
Bioinformatics, Biostatistics, Genetics
Heidelberg, Baden-Württemberg/Germany | Germany
Michael Fuchs
Michael Fuchs
University Hospital of Cologne
Germany
Sabine Ponader
Sabine Ponader
University of Erlangen-Nuremberg
Germany
Lewin Eisele
Lewin Eisele
Institute for Medical Informatics
Germany
Stefan Herms
Stefan Herms
Institute of Human Genetics
Germany

Eur J Hum Genet 2015 Jun 17;23(6):824-30. Epub 2014 Sep 17.

1] German Cancer Research Center (DKFZ), Division of Molecular Genetic Epidemiology, Heidelberg, Germany [2] Center for Primary Health Care Research, Lund University, Malmö, Sweden.

Genome-wide association studies (GWASs) have identified several single-nucleotide polymorphisms (SNPs) influencing the risk of Hodgkin's lymphoma (HL) and demonstrated the association of common genetic variation for this type of cancer. Such evidence for inherited genetic risk is also provided by the family history and the very high concordance between monozygotic twins. However, little is known about the genetic and environmental contributions. A common measure for describing the phenotypic variation due to genetics is the heritability. Using GWAS data on 906 HL cases by considering all typed SNPs simultaneously, we have calculated that the common variance explained by SNPs accounts for >35% of the total variation on the liability scale in HL (95% confidence interval 6-62%). These findings are consistent with similar heritability estimates of ∼ 0.40 (95% confidence interval 0.17-0.58) based on Swedish population data. Our estimates support the underlying polygenic basis for susceptibility to HL, and show that heritability based on the population data is somehow larger than heritability based on the genomic data because of the possibility of some missing heritability in the GWAS data. Besides that there is still major evidence for multiple loci causing HL on chromosomes other than chromosome 6 that need to be detected. Because of limited findings in prior GWASs, it seems worth checking for more loci causing susceptibility to HL.

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http://dx.doi.org/10.1038/ejhg.2014.184DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4795060PMC

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June 2015
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References

(Supplied by CrossRef)
Article in Cancer Epidemiol Biomarkers Prev
Hemminki K et al.
Cancer Epidemiol Biomarkers Prev 2002

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