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These studies have consistently implicated variation in the immune gene, human leucocyte antigen (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>), to be associated with lymphoma risk. In this review, we summarize the historical and recent evidence of <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> in both lymphoma aetiology and survival. The recent momentum in uncovering <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> associations has been propelled by the conduct of genome\u2010wide association studies (<jats:styled-content style=\"fixed-case\">GWAS<\/jats:styled-content>), which has permitted the evaluation of imputed <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> alleles in much larger sample sizes than historically feasible with allelotyping studies. Based on the culmination of smaller <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> typing studies and larger <jats:styled-content style=\"fixed-case\">GWAS<\/jats:styled-content>, we now recognize several <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> associations with Hodgkin (<jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content>) and non\u2010Hodgkin lymphomas (<jats:styled-content style=\"fixed-case\">NHL<\/jats:styled-content>s) and their subtypes. Although other genetic variants have also been implicated with lymphoma risk, it is notable that <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> associations have been reported in every <jats:styled-content style=\"fixed-case\">NHL<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> subtype evaluated to date. Both <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> class I and class <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> alleles have been linked with <jats:styled-content style=\"fixed-case\">NHL<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> risk. It is notable that the associations identified are largely specific to each lymphoma subtype. However, pleiotropic <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> associations have also been observed. For example, rs10484561, which is in linkage disequilibrium with <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*01:01\u02dc<jats:styled-content style=\"fixed-case\">DQA<\/jats:styled-content>1*01:01\u02dc<jats:styled-content style=\"fixed-case\">DQB<\/jats:styled-content>1*05:01<\/jats:italic>, has been implicated in increased <jats:styled-content style=\"fixed-case\">FL<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">DLBCL<\/jats:styled-content> risk. Opposing <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> associations across subtypes have also been reported, such as for <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010A*01:01<\/jats:italic> which is associated with increased risk of <jats:styled-content style=\"fixed-case\">EBV<\/jats:styled-content>\u2010positive <jats:styled-content style=\"fixed-case\">cHL<\/jats:styled-content> but decreased risk of <jats:styled-content style=\"fixed-case\">EBV<\/jats:styled-content>\u2010negative <jats:styled-content style=\"fixed-case\">cHL<\/jats:styled-content> and chronic lymphocytic leukaemia\/small cell lymphoma. Due to extensive linkage disequilibrium and allele\/haplotypic variation across race\/ethnicities, identification of causal alleles\/haplotypes remains challenging. Follow\u2010up functional studies are needed to identify the specific immunological pathways responsible in the multifactorial aetiology of <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NHL<\/jats:styled-content>. Correlative studies linking <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> alleles with known molecular subtypes and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> expression in the tumours are also needed. Finally, additional association studies investigating <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> diversity and lymphoma survival are also required to replicate initial associations reported to date.<\/jats:p>","DOI":"10.1111\/joim.12911","type":"journal-article","created":{"date-parts":[[2019,6,3]],"date-time":"2019-06-03T07:46:51Z","timestamp":1559548011000},"page":"154-180","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["The role of <scp>HLA<\/scp> variation in lymphoma aetiology and survival"],"prefix":"10.1111","volume":"286","author":[{"given":"C.","family":"Zhong","sequence":"first","affiliation":[{"name":"Division of Health Analytics, Department of Computational and Quantitative Medicine Beckman Research Institute and Comprehensive Cancer Center City of Hope Duarte CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.","family":"Cozen","sequence":"additional","affiliation":[{"name":"Genetic Epidemiology Center, Department of Preventive Medicine Keck School of Medicine of USC, USC Norris Comprehensive Cancer Center, University of Southern California Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Bolanos","sequence":"additional","affiliation":[{"name":"Genetic Epidemiology Center, Department of Preventive Medicine Keck School of Medicine of USC, USC Norris Comprehensive Cancer Center, University of Southern California Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Pathology City of Hope National Medical Center Duarte CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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