HLA class I and II diversity contributes to the etiologic heterogeneity of non-Hodgkin lymphoma subtypes

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F18%3A00078017" target="_blank" >RIV/00209805:_____/18:00078017 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/18:00106857

Výsledek na webu

<a href="http://cancerres.aacrjournals.org/content/78/14/4086.full-text.pdf" target="_blank" >http://cancerres.aacrjournals.org/content/78/14/4086.full-text.pdf</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1158/0008-5472.CAN-17-2900" target="_blank" >10.1158/0008-5472.CAN-17-2900</a>

Jazyk výsledku

angličtina

Název v původním jazyce

HLA class I and II diversity contributes to the etiologic heterogeneity of non-Hodgkin lymphoma subtypes

Popis výsledku v původním jazyce

A growing number of loci within the human leukocyte antigen (HLA) region have been implicated in non-Hodgkin lymphoma (NHL) etiology. Here, we test a complementary hypothesis of &quot;heterozygote advantage&quot; regarding the role of HLA and NHL, whereby HLA diversity is beneficial and homozygous HLA loci are associated with increased disease risk. HLA alleles at class I and II loci were imputed from genome-wide association studies (GWAS) using SNP2HLA for 3,617 diffuse large B-cell lymphomas (DLBCL), 2,686 follicular lymphomas (FL), 2,878 chronic lymphocytic leukemia/small lymphocytic lymphomas (CLL/SLL), 741 marginal zone lymphomas (MZL), and 8,753 controls of European descent. Both DLBCL and MZL risk were elevated with homozygosity at class I HLA-B and -C loci (OR DLBCL 1/4 1.31, 95% CI 1/4 1.06-1.60; OR MZL 1/4 1.45, 95% CI 1/4 1.12-1.89) and class II HLA-DRB1 locus (OR DLBCL 1/4 2.10, 95% CI 1/4 1.24-3.55; OR MZL 1/4 2.10, 95% CI 1/4 0.99-4.45). Increased FL risk was observed with the overall increase in number of homozygous HLA class II loci (P trend &lt; 0.0001, FDR 1/4 0.0005). These results support a role for HLA zygosity in NHL etiology and suggests that distinct immune pathways may underly the etiology of the different NHL subtypes. Significance: HLA gene diversity reduces risk for non-Hodgkin lymphoma.

Název v anglickém jazyce

HLA class I and II diversity contributes to the etiologic heterogeneity of non-Hodgkin lymphoma subtypes

Popis výsledku anglicky

A growing number of loci within the human leukocyte antigen (HLA) region have been implicated in non-Hodgkin lymphoma (NHL) etiology. Here, we test a complementary hypothesis of &quot;heterozygote advantage&quot; regarding the role of HLA and NHL, whereby HLA diversity is beneficial and homozygous HLA loci are associated with increased disease risk. HLA alleles at class I and II loci were imputed from genome-wide association studies (GWAS) using SNP2HLA for 3,617 diffuse large B-cell lymphomas (DLBCL), 2,686 follicular lymphomas (FL), 2,878 chronic lymphocytic leukemia/small lymphocytic lymphomas (CLL/SLL), 741 marginal zone lymphomas (MZL), and 8,753 controls of European descent. Both DLBCL and MZL risk were elevated with homozygosity at class I HLA-B and -C loci (OR DLBCL 1/4 1.31, 95% CI 1/4 1.06-1.60; OR MZL 1/4 1.45, 95% CI 1/4 1.12-1.89) and class II HLA-DRB1 locus (OR DLBCL 1/4 2.10, 95% CI 1/4 1.24-3.55; OR MZL 1/4 2.10, 95% CI 1/4 0.99-4.45). Increased FL risk was observed with the overall increase in number of homozygous HLA class II loci (P trend &lt; 0.0001, FDR 1/4 0.0005). These results support a role for HLA zygosity in NHL etiology and suggests that distinct immune pathways may underly the etiology of the different NHL subtypes. Significance: HLA gene diversity reduces risk for non-Hodgkin lymphoma.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

<a href="/cs/project/LO1413" target="_blank" >LO1413: RECAMO2020</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Cancer research

ISSN

0008-5472

e-ISSN

—

Svazek periodika

78

Číslo periodika v rámci svazku

14

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

4086-4096

Kód UT WoS článku

000439199100028

EID výsledku v databázi Scopus

2-s2.0-85050829279