Karin E Smedby1, Joshua N Sampson2, Jennifer J Turner2, Susan L Slager2, Marc Maynadié2, Eve Roman2, Thomas M Habermann2, Christopher R Flowers2, Sonja I Berndt2, Paige M Bracci2, Henrik Hjalgrim2, Dennis D Weisenburger2, Lindsay M Morton2. 1. Unit of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (KES); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (JNS, SIB, LMM); Department of Histopathology, Douglass Hanly Moir Pathology, Macquarie Park, Australia The Australian, School of Advanced Medicine, Macquarie University, Sydney, Australia (JJT); Department of Health Sciences Research, Mayo Clinic, Rochester, MN (SLS, TMH); Biological Hematology Unit; CRB Ferdinand Cabanne, University Hospital of Dijon, Dijon, France, EA4184, University of Burgundy, Dijon, France (MM); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (ER); Winship Cancer Institute, Emory University, Atlanta, GA (CRF); Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA (PMB); Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark (HH); Department of Pathology, City of Hope National Medical Center, Duarte, CA (DDW). karin.ekstrom.smedby@ki.se. 2. Unit of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (KES); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (JNS, SIB, LMM); Department of Histopathology, Douglass Hanly Moir Pathology, Macquarie Park, Australia The Australian, School of Advanced Medicine, Macquarie University, Sydney, Australia (JJT); Department of Health Sciences Research, Mayo Clinic, Rochester, MN (SLS, TMH); Biological Hematology Unit; CRB Ferdinand Cabanne, University Hospital of Dijon, Dijon, France, EA4184, University of Burgundy, Dijon, France (MM); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (ER); Winship Cancer Institute, Emory University, Atlanta, GA (CRF); Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA (PMB); Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark (HH); Department of Pathology, City of Hope National Medical Center, Duarte, CA (DDW).
Abstract
BACKGROUND: The etiology of mantle cell lymphoma (MCL), a distinctive subtype accounting for 2%-10% of all non-Hodgkin lymphoma, is not known. METHODS: We investigated associations with self-reported medical history, lifestyle, family history, and occupational risk factors in a pooled analysis of 557 patients with MCL and 13766 controls from 13 case-control studies in Europe, North America, and Australia. Odds ratios (ORs) and 95% confidence intervals (CIs) associated with each exposure were examined using multivariate logistic regression models. RESULTS: The median age of the MCL patients was 62 years and 76% were men. Risk of MCL was inversely associated with history of hay fever (OR = 0.63, 95% CI = 0.48 to 0.82), and the association was independent of other atopic diseases and allergies. A hematological malignancy among first-degree relatives was associated with a twofold increased risk of MCL (OR = 1.99, 95% CI = 1.39 to 2.84), which was stronger in men (OR = 2.21, 95% CI = 1.44 to 3.38) than women (OR = 1.61, 95% CI = 0.82 to 3.19). A modestly increased risk of MCL was also observed in association with ever having lived on a farm (OR = 1.40, 95% CI = 1.03 to 1.90). Unlike some other non-Hodgkin lymphoma subtypes, MCL risk was not statistically significantly associated with autoimmune disorders, tobacco smoking, alcohol intake, body mass index, or ultraviolet radiation. CONCLUSIONS: The novel observations of a possible role for atopy and allergy and farm life in risk of MCL, together with confirmatory evidence of a familial link, suggest a multifactorial etiology of immune-related environmental exposures and genetic susceptibility. These findings provide guidance for future research in MCL etiology. Published by Oxford University Press 2014.
BACKGROUND: The etiology of mantle cell lymphoma (MCL), a distinctive subtype accounting for 2%-10% of all non-Hodgkin lymphoma, is not known. METHODS: We investigated associations with self-reported medical history, lifestyle, family history, and occupational risk factors in a pooled analysis of 557 patients with MCL and 13766 controls from 13 case-control studies in Europe, North America, and Australia. Odds ratios (ORs) and 95% confidence intervals (CIs) associated with each exposure were examined using multivariate logistic regression models. RESULTS: The median age of the MCLpatients was 62 years and 76% were men. Risk of MCL was inversely associated with history of hay fever (OR = 0.63, 95% CI = 0.48 to 0.82), and the association was independent of other atopic diseases and allergies. A hematological malignancy among first-degree relatives was associated with a twofold increased risk of MCL (OR = 1.99, 95% CI = 1.39 to 2.84), which was stronger in men (OR = 2.21, 95% CI = 1.44 to 3.38) than women (OR = 1.61, 95% CI = 0.82 to 3.19). A modestly increased risk of MCL was also observed in association with ever having lived on a farm (OR = 1.40, 95% CI = 1.03 to 1.90). Unlike some other non-Hodgkin lymphoma subtypes, MCL risk was not statistically significantly associated with autoimmune disorders, tobacco smoking, alcohol intake, body mass index, or ultraviolet radiation. CONCLUSIONS: The novel observations of a possible role for atopy and allergy and farm life in risk of MCL, together with confirmatory evidence of a familial link, suggest a multifactorial etiology of immune-related environmental exposures and genetic susceptibility. These findings provide guidance for future research in MCL etiology. Published by Oxford University Press 2014.
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