Susan L Slager1, Yolanda Benavente2, Aaron Blair2, Roel Vermeulen2, James R Cerhan2, Adele Seniori Costantini2, Alain Monnereau2, Alexandra Nieters2, Jacqueline Clavel2, Timothy G Call2, Marc Maynadié2, Qing Lan2, Christina A Clarke2, Tracy Lightfoot2, Aaron D Norman2, Joshua N Sampson2, Delphine Casabonne2, Pierluigi Cocco2, Silvia de Sanjosé2. 1. Health Sciences Research, College of Medicine, Mayo Clinic, Rochester, MN (SLS, JRC, TGC, ADN); Unit of Infections and Cancer, Cancer Epidemiology Research Programme, Institut Català d' Oncologia, IDIBELL, L'Hospitalet de Llobregat, Spain, CIBER de Epidemiología y Salud Pública, Barcelona, Spain (YB, DC, SdS); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (AB, QL, JNS); Institute for Risk Assessment Sciences, Utrecht University, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands (RV); Unit of Occupational and Environmental Epidemiology, Cancer Prevention and Research Institute ISPO, Florence, Italy (ASC); Inserm, Centre for Research in Epidemiology and Population Health, Environmental Epidemiology of Cancer Group, Univ Paris Sud, Villejuif, France (AM, JC); Registry of Hematological Malignancies, Gironde and Bergonié Institute, Bordeaux, France (AM); Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg, Freiburg, Germany (AN); Biological Hematology Unit; CRB Ferdinand Cabanne, University Hospital of Dijon, University of Burgundy, France (MM); Cancer Prevention Institute of California, Fremont, CA (CAC); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (TL); Department of Public Health, Clinical and Molecular Medicine, Occupational Health Section, University of Cagliari, Cagliari, Italy (PC). slager@mayo.edu. 2. Health Sciences Research, College of Medicine, Mayo Clinic, Rochester, MN (SLS, JRC, TGC, ADN); Unit of Infections and Cancer, Cancer Epidemiology Research Programme, Institut Català d' Oncologia, IDIBELL, L'Hospitalet de Llobregat, Spain, CIBER de Epidemiología y Salud Pública, Barcelona, Spain (YB, DC, SdS); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (AB, QL, JNS); Institute for Risk Assessment Sciences, Utrecht University, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands (RV); Unit of Occupational and Environmental Epidemiology, Cancer Prevention and Research Institute ISPO, Florence, Italy (ASC); Inserm, Centre for Research in Epidemiology and Population Health, Environmental Epidemiology of Cancer Group, Univ Paris Sud, Villejuif, France (AM, JC); Registry of Hematological Malignancies, Gironde and Bergonié Institute, Bordeaux, France (AM); Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg, Freiburg, Germany (AN); Biological Hematology Unit; CRB Ferdinand Cabanne, University Hospital of Dijon, University of Burgundy, France (MM); Cancer Prevention Institute of California, Fremont, CA (CAC); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (TL); Department of Public Health, Clinical and Molecular Medicine, Occupational Health Section, University of Cagliari, Cagliari, Italy (PC).
Abstract
BACKGROUND: Chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL) are two subtypes of non-Hodgkin lymphoma. A number of studies have evaluated associations between risk factors and CLL/SLL risk. However, these associations remain inconsistent or lacked confirmation. This may be due, in part, to the inadequate sample size of CLL/SLL cases. METHODS: We performed a pooled analysis of 2440 CLL/SLL cases and 15186 controls from 13 case-control studies from Europe, North America, and Australia. We evaluated associations of medical history, family history, lifestyle, and occupational risk factors with CLL/SLL risk. Multivariate logistic regression analyses were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: We confirmed prior inverse associations with any atopic condition and recreational sun exposure. We also confirmed prior elevated associations with usual adult height, hepatitis C virus seropositivity, living or working on a farm, and family history of any hematological malignancy. Novel associations were identified with hairdresser occupation (OR = 1.77, 95% CI = 1.05 to 2.98) and blood transfusion history (OR = 0.79, 95% CI = 0.66 to 0.94). We also found smoking to have modest protective effect (OR = 0.9, 95% CI = 0.81 to 0.99). All exposures showed evidence of independent effects. CONCLUSIONS: We have identified or confirmed several independent risk factors for CLL/SLL supporting a role for genetics (through family history), immune function (through allergy and sun), infection (through hepatitis C virus), and height, and other pathways of immune response. Given that CLL/SLL has more than 30 susceptibility loci identified to date, studies evaluating the interaction among genetic and nongenetic factors are warranted. Published by Oxford University Press 2014.
BACKGROUND:Chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL) are two subtypes of non-Hodgkin lymphoma. A number of studies have evaluated associations between risk factors and CLL/SLL risk. However, these associations remain inconsistent or lacked confirmation. This may be due, in part, to the inadequate sample size of CLL/SLL cases. METHODS: We performed a pooled analysis of 2440 CLL/SLL cases and 15186 controls from 13 case-control studies from Europe, North America, and Australia. We evaluated associations of medical history, family history, lifestyle, and occupational risk factors with CLL/SLL risk. Multivariate logistic regression analyses were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: We confirmed prior inverse associations with any atopic condition and recreational sun exposure. We also confirmed prior elevated associations with usual adult height, hepatitis C virus seropositivity, living or working on a farm, and family history of any hematological malignancy. Novel associations were identified with hairdresser occupation (OR = 1.77, 95% CI = 1.05 to 2.98) and blood transfusion history (OR = 0.79, 95% CI = 0.66 to 0.94). We also found smoking to have modest protective effect (OR = 0.9, 95% CI = 0.81 to 0.99). All exposures showed evidence of independent effects. CONCLUSIONS: We have identified or confirmed several independent risk factors for CLL/SLL supporting a role for genetics (through family history), immune function (through allergy and sun), infection (through hepatitis C virus), and height, and other pathways of immune response. Given that CLL/SLL has more than 30 susceptibility loci identified to date, studies evaluating the interaction among genetic and nongenetic factors are warranted. Published by Oxford University Press 2014.
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