Infectious mononucleosis, immune genotypes, and non-Hodgkin lymphoma (NHL): an InterLymph Consortium study

• Type of Material: Article
• Authors: Niquelle Wade, University of Southern California; Cindy M. Chang, Food and Drug Administration; David Conti, University of Southern California; Joshua Millstein, University of Southern California; Christine Skibola, Emory University; Alexandra Nieters, University of Freiburg; Sophia S. Wang, City Hope Comprehensive Cancer Center; Silvia De Sanjose, Sexual & Reproductive Health; Eleanor Kane, University of York; John J. Spinelli, University of British Columbia; Paige Bracci, University of California San Francisco; Yawei Zhang, Yale University; Susan Slager, Mayo Clinic; Jun Wang, University of Southern California; Henrik Hjalgrim, Statens Serum Institut; Karin Ekstrom Smedby, Karolinska University; Elizabeth E. Brown, University of Alabama Birmingham; Ruth F. Jarrett, University of Glasgow; Wendy Cozen, University of Southern California
• Language: English
• Date: 2020-03-02
• Publisher: Springer
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © Springer Nature Switzerland AG 2020.
• Final Published Version (URL): http://dx.doi.org/10.1007/s10552-020-01266-4
• Title of Journal or Parent Work: Cancer Causes & Control
• Volume: 31
• Issue: 5
• Start Page: 451
• End Page: 462
• Grant/Funding Information: Agència de Gestió d’Ajuts Universitaris i de Recerca (AGAUR), CERCA Programme/Generalitat de Catalunya for institutional support (2017SGR1085); Spanish Ministry of Economy and Competitiveness—Carlos III Institute of Health cofunded by FEDER funds/European Regional Development Fund (ERDF)—a way to build Europe (PI14/01219);; National Cancer Institute’s Surveillance, Epidemiology, and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California (NHL MultiCenter Case-Control Study site), and contract HHSN261201000034C awarded to the Public Health Institute.; Centers for Disease Control and Prevention’s (CDC) National Program of Cancer Registries, under cooperative agreement 5NU58DP003862-04/DP003862;; This work was supported by awards from National Cancer Institute/National Institutes of Health (N01-CN-75014-20, P30CA014089, R01 CA186646, P30 CA13148, R21 CA155951, U54 CA118948, CA45614, CA87014, CA104682, and CA154643);; Centro de Investigación Biomédica en Red: Epidemiología y Salud Pública (CIBERESP, Spain); the Canadian Institutes for Health Research (CIHR); Canadian Cancer Society; and Michael Smith Foundation for Health Research [British Columbia]).; The collection of cancer incidence data used in the UCSF study was supported by the California Department of Public Health pursuant to California Health and Safety Code Section 103885
• Keywords: Polymorphisms; Genetic variation; Interleukin-1beta (IL1B); Risk; Public, Environmental & Occupational Health; T-cell lymphoma; Pooled analysis; Life Sciences & Biomedicine; Gene-environment interaction; Infectious mononucleosis; Medical history; Epstein Barr virus; T-cell lymphomas; HLA class I; Interleukin-6 (IL6); Inflammation genes; Oncology; Science & Technology; Non-Hodgkin lymphoma; Epidemiologic research
• Research Categories: Health Sciences, Epidemiology; Health Sciences, Public Health; Health Sciences, Oncology; Biology, Genetics

Abstract

Purpose We explored the interaction between non-Hodgkin lymphoma (NHL), infectious mononucleosis (IM) history, and immune-related genotypes in a pooled case–control analysis. Methods A total of 7,926 NHL patients and 10,018 controls from 12 case–control studies were included. Studies were conducted during various time periods between 1988 and 2008, and participants were 17–96 years of age at the time of ascertainment/recruitment. Self-reported IM history and immune response genotypes were provided by the InterLymph Data Coordinating Center at Mayo Clinic. Odds ratios (OR) were estimated using multivariate logistic regression, and interactions were estimated using the empirical Bayes method. PACT was used to account for multiple comparisons. Results There was evidence of an interaction effect between IM history and two variants on T-cell lymphoma (TCL) risk: rs1143627 in interleukin-1B (IL1B) (pinteraction = 0.04, ORinteraction = 0.09, 95% confidence interval [CI] 0.01, 0.87) and rs1800797 in interleukin-6 (IL6) (pinteraction = 0.03, ORinteraction = 0.08, 95% CI 0.01, 0.80). Neither interaction effect withstood adjustment for multiple comparisons. There were no statistically significant interactions between immune response genotypes and IM on other NHL subtypes. Conclusions Genetic risk variants in IL1B and IL6 may affect the association between IM and TCL, possibly by influencing T-cell activation, growth, and differentiation in the presence of IM, thereby decreasing risk of immune cell proliferation.