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

Thomsen, Hauke LU orcid ; da Silva Filho, Miguel Inacio ; Försti, Asta LU ; Fuchs, Michael ; Ponader, Sabine ; von Strandmann, Elke Pogge ; Eisele, Lewin ; Herms, Stefan ; Hofmann, Per and Sundquist, Jan LU , et al. (2015) In European Journal of Human Genetics 23(6). p.824-830
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... (More)
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.European Journal of Human Genetics advance online publication, 17 September 2014; doi:10.1038/ejhg.2014.184. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Human Genetics
volume
23
issue
6
pages
824 - 830
publisher
Nature Publishing Group
external identifiers
  • pmid:25227146
  • wos:000354474600023
  • scopus:84929271366
  • pmid:25227146
ISSN
1476-5438
DOI
10.1038/ejhg.2014.184
language
English
LU publication?
yes
id
eeb8c232-d055-4337-8c8d-5b5ab4a0745d (old id 4691412)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25227146?dopt=Abstract
date added to LUP
2016-04-01 10:02:57
date last changed
2022-04-19 22:11:26
@article{eeb8c232-d055-4337-8c8d-5b5ab4a0745d,
  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.European Journal of Human Genetics advance online publication, 17 September 2014; doi:10.1038/ejhg.2014.184.}},
  author       = {{Thomsen, Hauke and da Silva Filho, Miguel Inacio and Försti, Asta and Fuchs, Michael and Ponader, Sabine and von Strandmann, Elke Pogge and Eisele, Lewin and Herms, Stefan and Hofmann, Per and Sundquist, Jan and Engert, Andreas and Hemminki, Kari}},
  issn         = {{1476-5438}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{824--830}},
  publisher    = {{Nature Publishing Group}},
  series       = {{European Journal of Human Genetics}},
  title        = {{Heritability estimates on Hodgkin's lymphoma: a genomic- versus population-based approach.}},
  url          = {{http://dx.doi.org/10.1038/ejhg.2014.184}},
  doi          = {{10.1038/ejhg.2014.184}},
  volume       = {{23}},
  year         = {{2015}},
}