Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: a pooled analysis within the InterLymph consortium

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• 作者：Todd M. Gibson (1) (2)
  Karin E. Smedby (3)
  Christine F. Skibola (4)
  David W. Hein (5)
  Susan L. Slager (6)
  Silvia de Sanjosé (7) (8)
  Claire M. Vajdic (10) (9)
  Yawei Zhang (11)
  Brian C.-H. Chiu (12)
  Sophia S. Wang (13)
  Henrik Hjalgrim (14)
  Alexandra Nieters (15)
  Paige M. Bracci (16)
  Anne Kricker (17)
  Tongzhang Zheng (11)
  Carol Kolar (18)
  James R. Cerhan (6)
  Hatef Darabi (19)
  Nikolaus Becker (20)
  Lucia Conde (4)
  Theodore R. Holford (11)
  Dennis D. Weisenburger (21)
  Anneclaire J. De Roos (22) (23)
  Katja Butterbach (20)
  Jacques Riby (4)
  Wendy Cozen (24)
  Yolanda Benavente (7)
  Casey Palmers (4)
  Elizabeth A. Holly (16)
  Joshua N. Sampson (1)
  Nathaniel Rothman (1)
  Bruce K. Armstrong (17)
  Lindsay M. Morton (1)
  
• 关键词：Non ; Hodgkin lymphoma ; Gene environment interaction ; Cigarette smoking ; N ; acetyltransferase ; Follicular lymphoma
• 刊名：Cancer Causes and Control
• 出版年：2013
• 出版时间：January 2013
• 年：2013
• 卷：24
• 期：1
• 页码：125-134
• 全文大小：215KB
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• 作者单位：Todd M. Gibson (1) (2)
  Karin E. Smedby (3)
  Christine F. Skibola (4)
  David W. Hein (5)
  Susan L. Slager (6)
  Silvia de Sanjosé (7) (8)
  Claire M. Vajdic (10) (9)
  Yawei Zhang (11)
  Brian C.-H. Chiu (12)
  Sophia S. Wang (13)
  Henrik Hjalgrim (14)
  Alexandra Nieters (15)
  Paige M. Bracci (16)
  Anne Kricker (17)
  Tongzhang Zheng (11)
  Carol Kolar (18)
  James R. Cerhan (6)
  Hatef Darabi (19)
  Nikolaus Becker (20)
  Lucia Conde (4)
  Theodore R. Holford (11)
  Dennis D. Weisenburger (21)
  Anneclaire J. De Roos (22) (23)
  Katja Butterbach (20)
  Jacques Riby (4)
  Wendy Cozen (24)
  Yolanda Benavente (7)
  Casey Palmers (4)
  Elizabeth A. Holly (16)
  Joshua N. Sampson (1)
  Nathaniel Rothman (1)
  Bruce K. Armstrong (17)
  Lindsay M. Morton (1)
  
  1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., EPS 7090, Bethesda, MD, 20892, USA
  2. Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD, USA
  3. Unit of Clinical Epidemiology, Department of Medicine, Solna, Karolinska Institute, Stockholm, Sweden
  4. Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, CA, USA
  5. Department of Pharmacology and Toxicology and James Graham Brown Cancer Center, School of Medicine, University of Louisville, Louisville, KY, USA
  6. Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, MN, USA
  7. Unit of Infections and Cancer, Cancer Epidemiology Research Programme, Institut Català d’Oncologia, IDIBELL, Barcelona, Spain
  8. CIBER Epidemiologia y Salud Pública, Madrid, Spain
  10. Lowy Cancer Research Center, Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia
  9. Adult Cancer Program, University of New South Wales, Sydney, NSW, Australia
  11. Yale School of Public Health, Yale University, New Haven, CT, USA
  12. Department of Health Studies, University of Chicago, Chicago, IL, USA
  13. Division of Cancer Etiology, Department of Population Sciences, Beckman Research Institute and the City of Hope, Duarte, CA, USA
  14. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark
  15. Centre of Chronic Immunodeficiency, University Medical Center Freiburg, Freiburg, Germany
  16. Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, San Francisco, CA, USA
  17. School of Public Health, University of Sydney, Sydney, NSW, Australia
  18. The Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA
  19. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden
  20. Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany
  21. Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA
  22. Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, WA, USA
  23. Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA
  24. Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
  
• ISSN：1573-7225

文摘

Purpose Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case–control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95?% confidence intervals (95?% CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results Current smoking was associated with a significant 30?% increased risk of follicular lymphoma (n?=?1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95?% CI 1.07-.75) and intermediate/rapid (OR 1.27; 95?% CI 0.95-.69) acetylators (p interaction?=?0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.