Claire M Vajdic1, Ola Landgren2, Mary L McMaster2, Susan L Slager2, Angela Brooks-Wilson2, Alex Smith2, Anthony Staines2, Ahmet Dogan2, Stephen M Ansell2, Joshua N Sampson2, Lindsay M Morton2, Martha S Linet2. 1. Prince of Wales Clinical School, University of New South Wales, Sydney, Australia (CMV); Multiple Myeloma Section, Metabolism Branch (OL) and Division of Cancer Epidemiology and Genetics (MLM, JNS, LMM, MSL), National Cancer Institute, National Institutes of Health, Bethesda, MD; Department of Health Sciences Research, College of Medicine (SLS) and Division of Hematology (SMA), Mayo Clinic, Rochester, MN; Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada (AB-W); Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, BC, Canada (ABW); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, Heslington, York, UK (ASm); School of Nursing and Human Sciences, Dublin City University, Dublin, Leinster, Ireland (ASt); Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY (AD). claire.vajdic@unsw.edu.au. 2. Prince of Wales Clinical School, University of New South Wales, Sydney, Australia (CMV); Multiple Myeloma Section, Metabolism Branch (OL) and Division of Cancer Epidemiology and Genetics (MLM, JNS, LMM, MSL), National Cancer Institute, National Institutes of Health, Bethesda, MD; Department of Health Sciences Research, College of Medicine (SLS) and Division of Hematology (SMA), Mayo Clinic, Rochester, MN; Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada (AB-W); Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, BC, Canada (ABW); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, Heslington, York, UK (ASm); School of Nursing and Human Sciences, Dublin City University, Dublin, Leinster, Ireland (ASt); Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY (AD).
Abstract
BACKGROUND: Lymphoplasmacytic lymphoma/Waldenström's macroglobulinemia (LPL/WM), a rare non-Hodgkin lymphoma subtype, shows strong familial aggregation and a positive association with chronic immune stimulation, but evidence regarding other risk factors is very limited. METHODS: The International Lymphoma Epidemiology Consortium (InterLymph) pooled data from 11 predominantly population-based case-control studies from North America, Europe, and Australia to examine medical history, lifestyle, family history, and occupational risk factors for LPL/WM. Age-, sex-, race/ethnicity-, and study-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression for a total of 374 LPL/WM cases and 23 096 controls. RESULTS: In multivariate analysis including all putative risk factors, LPL/WM risk was associated with history of Sjögren's syndrome (OR = 14.0, 95% CI = 3.60 to 54.6), systemic lupus erythematosus (OR = 8.23, 95% CI = 2.69 to 25.2), hay fever (OR = 0.73, 95% CI = 0.54 to 0.99), positive hepatitis C serology (OR = 2.51, 95% CI = 1.03 to 6.17), hematologic malignancy in a first-degree relative (OR = 1.64, 95% CI = 1.02 to 2.64), adult weight (OR = 0.61, 95% CI = 0.44 to 0.85 for highest vs. lowest quartile), duration of cigarette smoking (OR = 1.46, 95% CI = 1.04 to 2.05 for ≥ 40 years vs. nonsmokers), and occupation as a medical doctor (OR = 5.54, 95% CI = 2.19 to 14.0). There was no association with other medical conditions, lifestyle factors, or occupations. CONCLUSIONS: This pooled analysis confirmed associations with immune conditions and family history of hematologic malignancy, and identified new associations with hay fever, weight, smoking, and occupation, and no association with other lifestyle factors. These findings offer clues to LPL/WM biology and prevention. Published by Oxford University Press 2014.
BACKGROUND: Lymphoplasmacytic lymphoma/Waldenström's macroglobulinemia (LPL/WM), a rare non-Hodgkin lymphoma subtype, shows strong familial aggregation and a positive association with chronic immune stimulation, but evidence regarding other risk factors is very limited. METHODS: The International Lymphoma Epidemiology Consortium (InterLymph) pooled data from 11 predominantly population-based case-control studies from North America, Europe, and Australia to examine medical history, lifestyle, family history, and occupational risk factors for LPL/WM. Age-, sex-, race/ethnicity-, and study-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression for a total of 374 LPL/WM cases and 23 096 controls. RESULTS: In multivariate analysis including all putative risk factors, LPL/WM risk was associated with history of Sjögren's syndrome (OR = 14.0, 95% CI = 3.60 to 54.6), systemic lupus erythematosus (OR = 8.23, 95% CI = 2.69 to 25.2), hay fever (OR = 0.73, 95% CI = 0.54 to 0.99), positive hepatitis C serology (OR = 2.51, 95% CI = 1.03 to 6.17), hematologic malignancy in a first-degree relative (OR = 1.64, 95% CI = 1.02 to 2.64), adult weight (OR = 0.61, 95% CI = 0.44 to 0.85 for highest vs. lowest quartile), duration of cigarette smoking (OR = 1.46, 95% CI = 1.04 to 2.05 for ≥ 40 years vs. nonsmokers), and occupation as a medical doctor (OR = 5.54, 95% CI = 2.19 to 14.0). There was no association with other medical conditions, lifestyle factors, or occupations. CONCLUSIONS: This pooled analysis confirmed associations with immune conditions and family history of hematologic malignancy, and identified new associations with hay fever, weight, smoking, and occupation, and no association with other lifestyle factors. These findings offer clues to LPL/WM biology and prevention. Published by Oxford University Press 2014.
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