Infectious mononucleosis, immune genotypes, and non-Hodgkin lymphoma (NHL): an InterLymph Consortium study
Supporting Files
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5 2020
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File Language:
English
Details
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Alternative Title:Cancer Causes Control
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Personal Author: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
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Description: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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Subjects:
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Keywords:
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Source:Cancer Causes Control. 31(5):451-462
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Pubmed ID:32124188
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Pubmed Central ID:PMC7534692
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Document Type:
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Funding:N01-CN-75014-20/CA/NCI NIH HHSUnited States/ ; HHSN261201000140C/CA/NCI NIH HHSUnited States/ ; HHSN261201000035C/CA/NCI NIH HHSUnited States/ ; U54 CA118948/CA/NCI NIH HHSUnited States/ ; UL1 TR001863/TR/NCATS NIH HHSUnited States/ ; R01-CA-186646/CA/NCI NIH HHSUnited States/ ; R21-CA-155951/CA/NCI NIH HHSUnited States/ ; R21 CA155951/CA/NCI NIH HHSUnited States/ ; U54-CA-118948/CA/NCI NIH HHSUnited States/ ; HHSN261201000035I/CA/NCI NIH HHSUnited States/ ; HHSN261201000034C/CA/NCI NIH HHSUnited States/ ; R01 CA087014/CA/NCI NIH HHSUnited States/ ; R01-CA-045614/CA/NCI NIH HHSUnited States/ ; P30 CA013148/CA/NCI NIH HHSUnited States/ ; R01-CA-104682/CA/NCI NIH HHSUnited States/ ; R01 CA186646/CA/NCI NIH HHSUnited States/ ; P30 CA014089/CA/NCI NIH HHSUnited States/ ; R01 CA154643/CA/NCI NIH HHSUnited States/ ; P30-CA-13148/CA/NCI NIH HHSUnited States/ ; P30-CA-014089/CA/NCI NIH HHSUnited States/ ; R01 CA104682/CA/NCI NIH HHSUnited States/ ; U58 DP003862/DP/NCCDPHP CDC HHSUnited States/ ; R01-CA-154643/CA/NCI NIH HHSUnited States/ ; R01 CA045614/CA/NCI NIH HHSUnited States/ ; MC_UU_12014/3/MRC_/Medical Research CouncilUnited Kingdom/
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Volume:31
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Issue:5
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Collection(s):
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Main Document Checksum:urn:sha256:c164a548eeb6ac6068d72af828d85d8fb5e8d30158223814bf09d8b275c19ca6
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Download URL:
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File Type:
Supporting Files
File Language:
English
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