Sophia S Wang1, Christopher R Flowers2, Marshall E Kadin2, Ellen T Chang2, Ann Maree Hughes2, Stephen M Ansell2, Andrew L Feldman2, Tracy Lightfoot2, Paolo Boffetta2, Mads Melbye2, Qing Lan2, Joshua N Sampson2, Lindsay M Morton2, Yawei Zhang2, Dennis D Weisenburger2. 1. Department of Cancer Etiology, Beckman Research Institute of the City of Hope, Duarte, CA (SSW); Winship Cancer Institute, Emory University, Atlanta, GA (CRF); Department of Dermatology, Boston University, Boston, MA, Roger Williams Medical Center, Providence, RI (MEK); Health Sciences Practice, Exponent, Inc., Menlo Park, CA, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ETC); National Centre for Epidemiology and Population Health, The Australian National University, Canberra, Australia (AMH); Department of Health Sciences Research, Mayo Clinic, Rochester, MN (SMA); Department of Laboratory Medicine and Pathology, Mayo Clinic Cancer Center, Rochester, MN (ALF); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (TL); Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY (PB); Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark (MM); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (QL, JNS, LMM); Department of Environmental Health Sciences, Yale School of Public Health, New Haven, CT (YZ); Department of Pathology, City of Hope National Medical Center, Duarte, CA (DDW). sowang@coh.org. 2. Department of Cancer Etiology, Beckman Research Institute of the City of Hope, Duarte, CA (SSW); Winship Cancer Institute, Emory University, Atlanta, GA (CRF); Department of Dermatology, Boston University, Boston, MA, Roger Williams Medical Center, Providence, RI (MEK); Health Sciences Practice, Exponent, Inc., Menlo Park, CA, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA (ETC); National Centre for Epidemiology and Population Health, The Australian National University, Canberra, Australia (AMH); Department of Health Sciences Research, Mayo Clinic, Rochester, MN (SMA); Department of Laboratory Medicine and Pathology, Mayo Clinic Cancer Center, Rochester, MN (ALF); Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK (TL); Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY (PB); Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark (MM); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (QL, JNS, LMM); Department of Environmental Health Sciences, Yale School of Public Health, New Haven, CT (YZ); Department of Pathology, City of Hope National Medical Center, Duarte, CA (DDW).
Abstract
BACKGROUND: Accounting for 10%-15% of all non-Hodgkin lymphomas in Western populations, peripheral T-cell lymphomas (PTCL) are the most common T-cell lymphoma but little is known about their etiology. Our aim was to identify etiologic risk factors for PTCL overall, and for specific PTCL subtypes, by analyzing data from 15 epidemiologic studies participating in the InterLymph Consortium. METHODS: A pooled analysis of individual-level data for 584 histologically confirmed PTCL cases and 15912 controls from 15 case-control studies conducted in Europe, North America, and Australia was undertaken. Data collected from questionnaires were harmonized to permit evaluation of a broad range of potential risk factors. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression. RESULTS: Risk factors associated with increased overall PTCL risk with a P value less than .05 included: a family history of hematologic malignancies (OR = 1.92, 95% CI = 1.30 to 2.84); celiac disease (OR = 17.8, 95% CI = 8.61 to 36.79); eczema (OR = 1.41, 95% CI = 1.07 to 1.85); psoriasis (OR = 1.97, 95% CI = 1.17 to 3.32); smoking 40 or more years (OR = 1.92, 95% CI = 1.41 to 2.62); and employment as a textile worker (ever) (OR = 1.58, 95% CI = 1.05 to 2.38) and electrical fitter (ever) (OR = 2.89, 95% CI = 1.41 to 5.95). Exposures associated with reduced overall PTCL risk included a personal history of allergies (OR = 0.69, 95% CI = 0.54 to 0.87), alcohol consumption (ever) (OR = 0.64, 95% CI = 0.49 to 0.82), and having ever lived or worked on a farm (OR = 0.72, 95% CI = 0.55% to 0.95%). We also observed the well-established risk elevation for enteropathy-type PTCL among those with celiac disease in our data. Conclusions Our pooled analyses identified a number of new potential risk factors for PTCL and require further validation in independent series. Published by Oxford University Press 2014.
BACKGROUND: Accounting for 10%-15% of all non-Hodgkin lymphomas in Western populations, peripheral T-cell lymphomas (PTCL) are the most common T-cell lymphoma but little is known about their etiology. Our aim was to identify etiologic risk factors for PTCL overall, and for specific PTCL subtypes, by analyzing data from 15 epidemiologic studies participating in the InterLymph Consortium. METHODS: A pooled analysis of individual-level data for 584 histologically confirmed PTCL cases and 15912 controls from 15 case-control studies conducted in Europe, North America, and Australia was undertaken. Data collected from questionnaires were harmonized to permit evaluation of a broad range of potential risk factors. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression. RESULTS: Risk factors associated with increased overall PTCL risk with a P value less than .05 included: a family history of hematologic malignancies (OR = 1.92, 95% CI = 1.30 to 2.84); celiac disease (OR = 17.8, 95% CI = 8.61 to 36.79); eczema (OR = 1.41, 95% CI = 1.07 to 1.85); psoriasis (OR = 1.97, 95% CI = 1.17 to 3.32); smoking 40 or more years (OR = 1.92, 95% CI = 1.41 to 2.62); and employment as a textile worker (ever) (OR = 1.58, 95% CI = 1.05 to 2.38) and electrical fitter (ever) (OR = 2.89, 95% CI = 1.41 to 5.95). Exposures associated with reduced overall PTCL risk included a personal history of allergies (OR = 0.69, 95% CI = 0.54 to 0.87), alcohol consumption (ever) (OR = 0.64, 95% CI = 0.49 to 0.82), and having ever lived or worked on a farm (OR = 0.72, 95% CI = 0.55% to 0.95%). We also observed the well-established risk elevation for enteropathy-type PTCL among those with celiac disease in our data. Conclusions Our pooled analyses identified a number of new potential risk factors for PTCL and require further validation in independent series. Published by Oxford University Press 2014.
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