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Eur J Hum Genet. 2015 Jun;23(6):824-30. doi: 10.1038/ejhg.2014.184. Epub 2014 Sep 17.

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

Author information

1
German Cancer Research Center (DKFZ), Division of Molecular Genetic Epidemiology, Heidelberg, Germany.
2
1] German Cancer Research Center (DKFZ), Division of Molecular Genetic Epidemiology, Heidelberg, Germany [2] Center for Primary Health Care Research, Lund University, Malmö, Sweden.
3
Department of Internal Medicine I, University Hospital of Cologne, Cologne, Germany.
4
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
5
1] Institute of Human Genetics and Department of Genomics, University of Bonn, Bonn, Germany [2] Division of Medical Genetics, Department of Biomedicine, University of Basel, Basel, Switzerland.
6
Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA, USA.

Abstract

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.

PMID:
25227146
PMCID:
PMC4795060
DOI:
10.1038/ejhg.2014.184
[Indexed for MEDLINE]
Free PMC Article

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