Heritability estimates on Hodgkin's lymphoma: a genomic- versus population-based approach.
(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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https://lup.lub.lu.se/record/4691412
- author
- organization
- publishing date
- 2015
- 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}}, }