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Cancer Research 69, 6482, August 15, 2009. Published Online First August 4, 2009;
doi: 10.1158/0008-5472.CAN-08-4372
© 2009 American Association for Cancer Research

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Epidemiology

Atopic Disease and Risk of Non–Hodgkin Lymphoma: An InterLymph Pooled Analysis

Claire M. Vajdic1, Michael O. Falster1,2, Silvia de Sanjose4,5, Otoniel Martínez-Maza6, Nikolaus Becker9, Paige M. Bracci10, Mads Melbye11, Karin Ekström Smedby12, Eric A. Engels13, Jennifer Turner3, Paolo Vineis14, Adele Seniori Costantini15, Elizabeth A. Holly10, Eleanor Kane16, John J. Spinelli17, Carlo La Vecchia18, Tongzhang Zheng19, Brian C-H. Chiu20, Luigino Dal Maso21, Pierluigi Cocco22, Marc Maynadié23, Lenka Foretova24, Anthony Staines25, Paul Brennan26, Scott Davis27, Richard Severson28, James R. Cerhan29, Elizabeth C. Breen7, Brenda Birmann30, Wendy Cozen8 and Andrew E. Grulich2

1 University of New South Wales Cancer Research Center, Prince of Wales Clinical School and 2 National Center in HIV Epidemiology and Clinical Research, University of New South Wales; 3 Department of Anatomical Pathology, St Vincent's Hospital, Sydney, Australia; 4 Epidemiologia i Registre del Càncer, Institut Català d' Oncologia; 5 CIBER Epidemiologia y Salud Publica, Barcelona, Spain; 6 Departments of Obstetrics and Gynecology and Microbiology, Immunology and Molecular Genetics, University of California at Los Angeles AIDS Institute and Jonsson Comprehensive Cancer Center and 7 Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California at Los Angeles; 8 Keck School of Medicine, Department of Preventive Medicine, University of Southern California, Los Angeles, California; 9 Division of Clinical Epidemiology, German Cancer Research Center, Heidelberg, Germany; 10 Department of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, California; 11 Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark; 12 Department of Medicine, Clinical Epidemiology Unit and Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; 13 Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, Maryland; 14 Environmental Epidemiology, Imperial College London, London, United Kingdom; 15 Occupational and Environmental Epidemiology Unit, Institute for Study and Prevention of Cancer, Florence, Italy; 16 Epidemiology and Genetics Unit, Department of Health Sciences, University of York, York, United Kingdom; 17 Cancer Control Research Program, BC Cancer Agency, Vancouver, British Columbia, Canada; 18 Istituto di Ricerche Farmacologiche "Mario Negri" and Istituto di Statistica Medica e Biometria, Università degli Studi di Milano, Milan, Italy; 19 Department of Epidemiology and Public Health, Yale School of Medicine, New Haven, Connecticut; 20 Department of Health Studies, University of Chicago, Chicago, Illinois; 21 Epidemiology and Biostatistics Unit, Aviano Cancer Center, Aviano, Italy; 22 Department of Public Health, Occupational Health Section, University of Cagliari, Cagliari, Italy; 23 Registry of Hematological Malignancies of Cote d'Or, Dijon University Hospital, Dijon, France; 24 Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno, Czech Republic; 25 School of Nursing, Dublin City University, Dublin, Ireland; 26 IARC, Lyons, France; 27 Fred Hutchinson Cancer Research Center and School of Public Health and Community Medicine, University of Washington, Seattle, Washington; 28 Department of Family Medicine and Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan; 29 Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, Minnesota; and 30 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts

Requests for reprints: Claire M. Vajdic, University of New South Wales Cancer Research Center, Prince of Wales Clinical School, University of New South Wales, Level 1 South Wing Edmund Blacket Building, Prince of Wales Hospital, Randwick, New South Wales 2031, Australia. Phone: 61-2-9382-8881; Fax: 61-2-9382-8885; E-mail: claire.vajdic{at}unsw.edu.au.

Key Words: non–Hodgkin lymphoma • atopy • case-control • pooled analysis • risk

We performed a pooled analysis of data on atopic disease and risk of non–Hodgkin lymphoma (NHL) from 13 case-control studies, including 13,535 NHL cases and 16,388 controls. Self-reported atopic diseases diagnosed 2 years or more before NHL diagnosis (cases) or interview (controls) were analyzed. Pooled odds ratios (OR) and 95% confidence intervals (95% CI) were computed in two-stage random-effects or joint fixed-effects models, and adjusted for age, sex, and study center. When modeled individually, lifetime history of asthma, hay fever, specific allergy (excluding hay fever, asthma, and eczema), and food allergy were associated with a significant reduction in NHL risk, and there was no association for eczema. When each atopic condition was included in the same model, reduced NHL risk was only associated with a history of allergy (OR, 0.80; 95% CI, 0.68–0.94) and reduced B-cell NHL risk was associated with history of hay fever (OR, 0.85; 95% CI, 0.77–0.95) and allergy (OR, 0.84; 95% CI, 0.76–0.93). Significant reductions in B-cell NHL risk were also observed in individuals who were likely to be truly or highly atopic—those with hay fever, allergy, or asthma and at least one other atopic condition over their lifetime. The inverse associations were consistent for the diffuse large B-cell and follicular subtypes. Eczema was positively associated with lymphomas of the skin; misdiagnosis of lymphoma as eczema is likely, but progression of eczema to cutaneous lymphoma cannot be excluded. This pooled study shows evidence of a modest but consistent reduction in the risk of B-cell NHL associated with atopy. [Cancer Res 2009;69(16):6482–9]







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