• Je něco špatně v tomto záznamu ?

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

P. Khankhanian, W. Cozen, DS. Himmelstein, L. Madireddy, L. Din, A. van den Berg, T. Matsushita, SL. Glaser, JM. Moré, KE. Smedby, SE. Baranzini, TM. Mack, A. Lizée, S. de Sanjosé, PA. Gourraud, A. Nieters, SL. Hauser, P. Cocco, M. Maynadié, L....

. 2016 ; 45 (3) : 728-40. [pub] 20160312

Jazyk angličtina Země Velká Británie

Typ dokumentu časopisecké články, metaanalýza, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S., práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc18011282

BACKGROUND: 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, 9772 MS patients and 25 255 controls, we therefore investigated the genetic overlap between the two diseases. METHODS: 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. RESULTS: 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 R(2)), 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. CONCLUSIONS: HL displays considerable genetic overlap with MS and other autoimmune diseases.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc18011282
003      
CZ-PrNML
005      
20180417153524.0
007      
ta
008      
180404s2016 xxk f 000 0|eng||
009      
AR
024    7_
$a 10.1093/ije/dyv364 $2 doi
035    __
$a (PubMed)26971321
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxk
100    1_
$a Khankhanian, Pouya $u Center for Neuroengineering and Thereapeutics at the University of Pennsylvania, Philadelphia, PA, USA University of California, San Francisco, CA, USA.
245    10
$a Meta-analysis of genome-wide association studies reveals genetic overlap between Hodgkin lymphoma and multiple sclerosis / $c P. Khankhanian, W. Cozen, DS. Himmelstein, L. Madireddy, L. Din, A. van den Berg, T. Matsushita, SL. Glaser, JM. Moré, KE. Smedby, SE. Baranzini, TM. Mack, A. Lizée, S. de Sanjosé, PA. Gourraud, A. Nieters, SL. Hauser, P. Cocco, M. Maynadié, L. Foretová, A. Staines, M. Delahaye-Sourdeix, D. Li, S. Bhatia, M. Melbye, K. Onel, R. Jarrett, JD. McKay, JR. Oksenberg, H. Hjalgrim,
520    9_
$a BACKGROUND: 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, 9772 MS patients and 25 255 controls, we therefore investigated the genetic overlap between the two diseases. METHODS: 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. RESULTS: 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 R(2)), 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. CONCLUSIONS: HL displays considerable genetic overlap with MS and other autoimmune diseases.
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a genové regulační sítě $7 D053263
650    _2
$a genetická predispozice k nemoci $7 D020022
650    12
$a celogenomová asociační studie $7 D055106
650    _2
$a Hodgkinova nemoc $x genetika $7 D006689
650    _2
$a lidé $7 D006801
650    _2
$a lineární modely $7 D016014
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a roztroušená skleróza $x genetika $7 D009103
650    12
$a jednonukleotidový polymorfismus $7 D020641
655    _2
$a časopisecké články $7 D016428
655    _2
$a metaanalýza $7 D017418
655    _2
$a Research Support, N.I.H., Extramural $7 D052061
655    _2
$a Research Support, U.S. Gov't, Non-P.H.S. $7 D013486
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Cozen, Wendy $u University of Southern California, Los Angeles, CA, USA.
700    1_
$a Himmelstein, Daniel S $u University of California, San Francisco, CA, USA.
700    1_
$a Madireddy, Lohith $u University of California, San Francisco, CA, USA.
700    1_
$a Din, Lennox $u University of California, San Francisco, CA, USA.
700    1_
$a van den Berg, Anke $u University Medical Center, Groningen, The Netherlands.
700    1_
$a Matsushita, Takuya $u University of California, San Francisco, CA, USA.
700    1_
$a Glaser, Sally L $u Cancer Prevention Institute of California, Fremont, CA, USA.
700    1_
$a Moré, Jayaji M $u University of California, San Francisco, CA, USA.
700    1_
$a Smedby, Karin E $u Karolinska Institute, Stockholm, Sweden.
700    1_
$a Baranzini, Sergio E $u University of California, San Francisco, CA, USA.
700    1_
$a Mack, Thomas M $u University of Southern California, Los Angeles, CA, USA.
700    1_
$a Lizée, Antoine $u University of California, San Francisco, CA, USA.
700    1_
$a de Sanjosé, Silvia $u Catalan Institute of Oncology, L'Hospitalet de Llobregat, Catalonia, Spain.
700    1_
$a Gourraud, Pierre-Antoine $u University of California, San Francisco, CA, USA.
700    1_
$a Nieters, Alexandra $u University Medical Center Freiburg, Freiburg, Germany.
700    1_
$a Hauser, Stephen L $u University of California, San Francisco, CA, USA.
700    1_
$a Cocco, Pierluigi $u University of Cagliari, Cagliari, Sardinia, Italy.
700    1_
$a Maynadié, Marc $u Centre Hospitalier Universitaire de Dijon, Dijon, France.
700    1_
$a Foretová, Lenka $u Masaryk Memorial Cancer Institute, Brno, Czech Republic.
700    1_
$a Staines, Anthony $u University College Dublin, Dublin, Ireland.
700    1_
$a Delahaye-Sourdeix, Manon $u International Agency for Research on Cancer, Lyon, France.
700    1_
$a Li, Dalin $u University of Southern California, Los Angeles, CA, USA.
700    1_
$a Bhatia, Smita $u City of Hope National Medical Center, Duarte, CA, USA.
700    1_
$a Melbye, Mads $u Statens Serum Institut, Copenhagen S, Denmark.
700    1_
$a Onel, Kenan $u University of Chicago, Chicago, IL, USA.
700    1_
$a Jarrett, Ruth $u MRC, University of Glasgow Centre for Virus Research, Glasgow, UK.
700    1_
$a McKay, James D $u International Agency for Research on Cancer, Lyon, France.
700    1_
$a Oksenberg, Jorge R $u University of California, San Francisco, CA, USA.
700    1_
$a Hjalgrim, Henrik $u Statens Serum Institut, Copenhagen S, Denmark HHJ@ssi.dk.
773    0_
$w MED00002316 $t International journal of epidemiology $x 1464-3685 $g Roč. 45, č. 3 (2016), s. 728-40
856    41
$u https://pubmed.ncbi.nlm.nih.gov/26971321 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20180404 $b ABA008
991    __
$a 20180417153623 $b ABA008
999    __
$a ok $b bmc $g 1288767 $s 1008094
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2016 $b 45 $c 3 $d 728-40 $e 20160312 $i 1464-3685 $m International journal of epidemiology $n Int J Epidemiol $x MED00002316
LZP    __
$a Pubmed-20180404

Najít záznam

Citační ukazatele

Možnosti archivace