Srikant Ambatipudi1, Cyrille Cuenin1, Hector Hernandez-Vargas1, Akram Ghantous1, Florence Le Calvez-Kelm1, Rudolf Kaaks2, Myrto Barrdahl2, Heiner Boeing3, Krasimira Aleksandrova3, Antonia Trichopoulou4,5, Pagona Lagiou4,5, Androniki Naska4,5, Domenico Palli6, Vittorio Krogh7, Silvia Polidoro8, Rosario Tumino9, Salvatore Panico10, Bas Bueno-de-Mesquita11,12,13,14, Petra Hm Peeters15,16, José Ramón Quirós17, Carmen Navarro18,19,20, Eva Ardanaz19,21,22, Miren Dorronsoro23, Tim Key24, Paolo Vineis25, Neil Murphy25, Elio Riboli25, Isabelle Romieu1, Zdenko Herceg1. 1. International Agency for Research on Cancer (IARC), Lyon, France. 2. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. 3. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. 4. Hellenic Health Foundation, Athens, Greece. 5. WHO Collaborating Center for Nutrition & Health, Unit of Nutritional Epidemiology & Nutrition in Public Health, Department of Hygiene, Epidemiology & Medical Statistics, University of Athens Medical School, Athens, Greece. 6. Molecular & Nutritional Epidemiology Unit, Cancer Research & Prevention Institute-ISPO, Florence, Italy. 7. Epidemiology & Prevention Unit, Fondazione IRCCS Istituto Nazionale Tumori, Milano, Italy. 8. Human Genetic Foundation (HuGeF), Torino, Italy. 9. Cancer Registry & Histopathology Unit, 'Civic MP Arezzo' Hospital, ASP Ragusa, Italy. 10. Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. 11. Department of Determinants of Chronic Diseases (DCD), National Institute for Public Health & the Environment (RIVM), Bilthoven, The Netherlands. 12. Department of Gastroenterology & Hepatology, University Medical Centre, Utrecht, The Netherlands. 13. Department of Epidemiology & Biostatistics, The School of Public Health, Imperial College London, London, UK. 14. Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. 15. Department of Epidemiology, Julius Center for Health Sciences & Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. 16. MRC-PHE Centre for Environment & Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, UK. 17. Public Health Directorate, Asturias, Spain. 18. Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain. 19. CIBER Epidemiología y Salud Pública (CIBERESP), Spain. 20. Department of Health & Social Sciences, Universidad de Murcia, Spain. 21. Public Health Institute of Navarra, Pamplona, Spain. 22. IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. 23. Public Health Direction and Biodonostia-Ciberesp, Basque Regional Health Department, San Sebastian, Spain. 24. Cancer Epidemiology Unit, University of Oxford, Oxford, UK. 25. School of Public Health, Imperial College London, London, UK.
Abstract
AIM: Epigenetic changes may occur in response to environmental stressors, and an altered epigenome pattern may represent a stable signature of environmental exposure. MATERIALS & METHODS: Here, we examined the potential of DNA methylation changes in 910 prediagnostic peripheral blood samples as a marker of exposure to tobacco smoke in a large multinational cohort. RESULTS: We identified 748 CpG sites that were differentially methylated between smokers and nonsmokers, among which we identified novel regionally clustered CpGs associated with active smoking. Importantly, we found a marked reversibility of methylation changes after smoking cessation, although specific genes remained differentially methylated up to 22 years after cessation. CONCLUSION: Our study has comprehensively cataloged the smoking-associated DNA methylation alterations and showed that these alterations are reversible after smoking cessation.
AIM: Epigenetic changes may occur in response to environmental stressors, and an altered epigenome pattern may represent a stable signature of environmental exposure. MATERIALS & METHODS: Here, we examined the potential of DNA methylation changes in 910 prediagnostic peripheral blood samples as a marker of exposure to tobacco smoke in a large multinational cohort. RESULTS: We identified 748 CpG sites that were differentially methylated between smokers and nonsmokers, among which we identified novel regionally clustered CpGs associated with active smoking. Importantly, we found a marked reversibility of methylation changes after smoking cessation, although specific genes remained differentially methylated up to 22 years after cessation. CONCLUSION: Our study has comprehensively cataloged the smoking-associated DNA methylation alterations and showed that these alterations are reversible after smoking cessation.
Entities:
Keywords:
DNA methylome; epigenetic signature; prospective cohort; tobacco smoking
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