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Meta-analysis of genome-wide association studies reveals genetic overlap between Hodgkin lymphoma and multiple sclerosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F16%3AN0000070" target="_blank" >RIV/00209805:_____/16:N0000070 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.ncbi.nlm.nih.gov/pubmed/26971321" target="_blank" >https://www.ncbi.nlm.nih.gov/pubmed/26971321</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1093/ije/dyv364" target="_blank" >10.1093/ije/dyv364</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Meta-analysis of genome-wide association studies reveals genetic overlap between Hodgkin lymphoma and multiple sclerosis

  • Original language description

    Based on epidemiological commonalities, multiple sclerosis (MS) and Hodgkin lymphoma (HL), two clinically distinct conditions, have long been suspected to be aetiologically related. MS and HL occur in roughly the same age groups, both are associated with Epstein-Barr virus infection and ultraviolet (UV) light exposure, and they cluster mutually in families (though not in individuals). We speculated if in addition to sharing environmental risk factors, MS and HL were also genetically related. Using data from genome-wide association studies (GWAS) of 1816 HL patients, 9772MS patiens and 25 255 controls, we therefore investigated the genetic overlap between the two diseases. From among a common denominator of 404 K single nucleotide polymorphisms (SNPs) studied, we identified SNPs and human leukocyte antigen (HLA) alleles independently associated with both diseases. Next, we assessed the cumulative genome-wide effect of MS-associated SNPs on HL and of HL-associated SNPs on MS. To provide an interpretational frame of reference, we used data from published GWAS to create a genetic network of diseases within which we analysed proximity of HL and MS to autoimmune diseases and haematological and non-haematological malignancies. SNP analyses revealed genome-wide overlap between HL and MS, most prominently in the HLA region. Polygenic HL risk scores explained 4.44% of HL risk (Nagelkerke R2), but also 2.36% of MS risk. Conversely, polygenic MS risk scores explained 8.08% of MS risk and 1.94% of HL risk. In the genetic disease network, HL was closer to autoimmune diseases than to solid cancers. HL displays considerable genetic overlap with MS and other autoimmune diseases.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FD - Oncology and haematology

  • OECD FORD branch

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    International Journal of Epidemiology

  • ISSN

    0300-5771

  • e-ISSN

  • Volume of the periodical

    45

  • Issue of the periodical within the volume

    3

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    13

  • Pages from-to

    728-740

  • UT code for WoS article

    000384653200027

  • EID of the result in the Scopus database