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Infectious mononucleosis, immune genotypes, and non-Hodgkin lymphoma (NHL): an InterLymph Consortium study.
Wadé, Niquelle Brown; Chang, Cindy M; Conti, David; Millstein, Joshua; Skibola, Christine; Nieters, Alexandra; Wang, Sophia S; De Sanjose, Silvia; Kane, Eleanor; Spinelli, John J; Bracci, Paige; Zhang, Yawei; Slager, Susan; Wang, Jun; Hjalgrim, Henrik; Smedby, Karin Ekstrom; Brown, Elizabeth E; Jarrett, Ruth F; Cozen, Wendy.
Afiliação
  • Wadé NB; Department of Preventive Medicine, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Chang CM; Cigna Health and Life Insurance Company (Cigna), Bloomfield, CT, USA.
  • Conti D; Division of Population Health Sciences, Center for Tobacco Products, Food and Drug Administration, Bethesda, MD, USA.
  • Millstein J; Department of Preventive Medicine, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Skibola C; USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Nieters A; Department of Preventive Medicine, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Wang SS; USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • De Sanjose S; Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, USA.
  • Kane E; Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg, University of Freiburg, Freiburg, Germany.
  • Spinelli JJ; Department of Computational and Quantitative Medicine, City of Hope Comprehensive Cancer Center, Duarte, CA, USA.
  • Bracci P; Sexual and Reproductive Health, PATH, Seattle, WA, USA.
  • Zhang Y; Centro de Investigación Biomédica en Red: Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.
  • Slager S; Department of Health Sciences, University of York, York, YO10 5DD, UK.
  • Wang J; Population Oncology, BC Cancer Agency, Vancouver, Canada.
  • Hjalgrim H; School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada.
  • Smedby KE; Department of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, CA, USA.
  • Brown EE; Department of Surgery, Yale School of Medicine and Yale School of Public Health, New Haven, CT, USA.
  • Jarrett RF; Department of Epidemiology, Mayo Clinic, Rochester, MN, USA.
  • Cozen W; Department of Preventive Medicine, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Cancer Causes Control ; 31(5): 451-462, 2020 05.
Article em En | MEDLINE | ID: mdl-32124188
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Linfoma não Hodgkin / Mononucleose Infecciosa Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Linfoma não Hodgkin / Mononucleose Infecciosa Idioma: En Ano de publicação: 2020 Tipo de documento: Article