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RESEARCH PRODUCT
Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes.
Paul BrennanM. G. EnnasQing LanSasha BernatskySasha BernatskyAlan A. ArslanPeter KraftLohith MadireddyRoel VermeulenKenan OnelGraham G. GilesGraham G. GilesJohn J. SpinelliJohn J. SpinelliEleanor KaneBengt GlimeliusAlexandra NietersDavid V. ContiChristine F. SkibolaPouya KhankhanianAmy MooreRuth C. TravisMads MelbyeMads MelbyeSonja I. BerndtMark LiebowLauren R. TerasPierluigi CoccoLennox DinAlain MonnereauMark P. PurdueLenka ForetovaStephen J. ChanockStephen M. AnsellAngela Brooks-wilsonAngela Brooks-wilsonWendy CozenKenneth OffitDemetrius AlbanesAnne J. NovakMelissa C. SoutheyMelissa C. SoutheyPaolo BoffettaNicola J. CampJames R. CerhanRudolph KaaksSilvia De SanjoséKaren CurtinSophia S. WangJames MckayNicole Wong DooNicole Wong DooHans-olov AdamiHans-olov AdamiTongzhang ZhengClaire M. VajdicNisha PradhanGiacomo MuziGilles SallesNathaniel RothmanYolanda BenaventeMarc MaynadiéBrian K. LinkDelphine CasabonneHervé GhesquièresJoseph VijaiKarin E. SmedbyPaige M. BracciDavid G. CoxBrenda M. BirmannLucia MiligiCarolyn StewartLucia CondeLeonid PadyukovEve RomanRichard K. SeversonJorge R. OksenbergImmaculata De VivoImmaculata De VivoYawei ZhangCorrado MagnaniJacqueline ClavelLindsay M. MortonCorinne HaiounJonathan N. HofmannKaren H. CostenbaderPierre-antoine GourraudPierre-antoine GourraudMohammad SheikhStephanie J. WeinsteinSusan L. SlagerPaolo VineisNikitha KosarajuZachary TaubHenrik HjalgrimRoger L. MilneRoger L. MilneRoger L. MilneMorris DinMartha GlennNikolaus BeckerTimothy J. VyseThomas M. MackAnthony Stainessubject
OncologyMaleMultifactorial InheritanceLymphomaEpidemiologyChronic lymphocytic leukemiaFollicular lymphomaGenome-wide association studyDiseaseNeurodegenerativemeta-analysiimmune system diseasesHLA AntigensRisk Factorshemic and lymphatic diseases2.1 Biological and endogenous factorsHLA AntigenAetiologyGenetics (clinical)CancerAllele0303 health sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyLymphoma Non-Hodgkinnon-Hodgkin lymphoma030305 genetics & hereditySingle NucleotideHematologyMiddle Aged3. Good healthnon-Hodgkin lymphoma.Public Health and Health ServicesFemaleHumanmedicine.medical_specialtyautoimmune disease; genome-wide association study; meta-analysis; non-Hodgkin lymphoma; Alleles; Autoimmune Diseases; Female; HLA Antigens; Humans; Lymphoma Non-Hodgkin; Male; Middle Aged; Multifactorial Inheritance; Polymorphism Single Nucleotide; Risk Factors; Genetic Predisposition to DiseaseNon-Hodgkinautoimmune diseasePolymorphism Single NucleotideArticleAutoimmune Diseases03 medical and health sciencesRare DiseasesInternal medicineGenetic variationmedicineGeneticsHumansGenetic Predisposition to DiseasePolymorphismAlleles030304 developmental biologyAutoimmune diseasegenome-wide association studybusiness.industryMultiple sclerosisRisk FactorArthritisInflammatory and immune systemHuman Genomemedicine.diseaseLymphomaBrain Disordersmeta-analysisbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologydescription
International audience; Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2019-08-13 |