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12 results on '"Vermeulen, Roel CH"'

1. Spirometric phenotypes from early childhood to young adulthood: a Chronic Airway Disease Early Stratification study

Author

Wang, Gang, Hallberg, Jenny, Charalampopoulos, Dimitrios, Sanahuja, Maribel Casas, Breyer-Kohansal, Robab, Langhammer, Arnulf, Granell, Raquel, Vonk, Judith M, Mian, Annemiek, Olvera, Nuria, Laustsen, Lisbeth Molgaard, Ronmark, Eva, Abellan, Alicia, Agusti, Alvar, Arshad, Syed Hasan, Bergstrom, Anna, Boezen, H Marike, Breyer, Marie-Kathrin, Burghuber, Otto, Bolund, Anneli Clea, Custovic, Adnan, Devereux, Graham, Donaldson, Gavin C, Duijts, Liesbeth, Esplugues, Ana, Faner, Rosa, Ballester, Ferran, Garcia-Aymerich, Judith, Gehring, Ulrike, Haider, Sadia, Hartl, Sylvia, Backman, Helena, Holloway, John W, Koppelman, Gerard H, Lertxundi, Aitana, Holmen, Turid Lingaas, Lowe, Lesley, Mensink-Bout, Sara M, Murray, Clare S, Roberts, Graham, Hedman, Linnea, Schlunssen, Vivi, Sigsgaard, Torben, Simpson, Angela, Sunyer, Jordi, Torrent, Maties, Turner, Stephen, Van den Berge, Maarten, Vermeulen, Roel CH, Vikjord, Sigrid Anna Aalberg, Wedzicha, Jadwiga A, van der Zee, Anke H Maitland, Melen, Erik, and Collaboration, CADSET Clinical Res

Published
2021

2. Diet, Physical Activity, and Daylight Exposure Patterns in Night-Shift Workers and Day Workers

Author

van de Langenberg, Daniella, Vlaanderen, Jelle J, Dollé, Martijn Et, Rookus, Matti A, van Kerkhof, Linda Wm, Vermeulen, Roel Ch, and One Health Chemisch

Subjects
circadian rhythm, shift work, exposure assessment, occupational health, physical activity, daylight exposure, dietary pattern, night work, chronobiology
Abstract

Background: Night-shift work has been reported to have an impact on nutrition, daylight exposure, and physical activity, which might play a role in observed health effects. Because these exposures show diurnal variation, and shift work has been related with disturbances in the circadian rhythm, the timing of assessment of these factors requires careful consideration. Our aim was to describe the changes in patterns of diet, physical activity, and daylight exposure associated with night-shift work. Methods: We conducted an observational study among female healthcare workers either regularly working night shifts or not working night shifts. We assessed physical activity and daylight exposure using continuous monitoring devices for 48 h. We logged dietary patterns (24 h) and other health- and work-associated characteristics. Two measurement sessions were conducted when participants did 'not' work night shifts, and one session was conducted during a night-shift period. Results: Our study included 69 night-shift workers and 21 day workers. On days in which they conduct work but no night work, night-shift workers had similar physical activity and 24-h caloric intake, yet higher overall daylight exposures than day workers and were more often exposed around noon instead of mainly around 1800h. Night-shift workers were less exposed to daylight during the night-shift session compared to the non-night-shift session. Total caloric intakes did not significantly differ between sessions, but we did observe a shorter maximum fasting interval, more eating moments, and a higher percentage of fat intake during the night-shift session. Conclusion: Observed differences in diet, physical activity, and exposure to daylight primarily manifested themselves through changes in exposure patterns, highlighting the importance of time-resolved measurements in night-shift-work research. Patterns in daylight exposure were primarily related to time of waking up and working schedule, whereas timing of dinner seemed primarily governed by social conventions.

Published
2020

3. Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia

Author

Law, Philip J, Berndt, Sonja I, Speedy, Helen E, Camp, Nicola J, Sava, Georgina P, Skibola, Christine F, Holroyd, Amy, Vijai, Joseph, Sunter, Nicola J, Nieters, Alexandra, Bea, Silvia, Pettitt, AR, Monnereau, Alain, Martin-Garcia, David, Goldin, Lynn R, Clot, Guillem, Teras, Lauren R, Quintela, Inés, Birmann, Brenda M, Jayne, Sandrine J, Cozen, Wendy, Majid, Aneela, Smedby, Karin E, Lan, Qing, Dearden, Claire, Brooks-Wilson, Angela R, Hall, Andrew G, Purdue, Mark P, Mainou-Fowler, Tryfonia, Vajdic, Claire M, Jackson, Graham H, Cocco, Pierluigi, Marr, Helen, Zhang, Yawei, Zheng, Tongzhang, Giles, Graham G, Lawrence, Charles, Call, Timothy G, Liebow, Mark, Melbye, Mads, Glimelius, Bengt, Mansouri, Larry, Glenn, Martha, Curtin, Karen, Diver, W Ryan, Link, Brian K, Conde, Lucia, Bracci, Paige M, Holly, Elizabeth A, Jackson, Rebecca D, Tinker, Lesley F, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Maynadie, Marc, Mckay, James, Albanes, Demetrius, Weinstein, Stephanie, Wang, Zhaoming, Caporaso, Neil E, Morton, Lindsay M, Severson, Richard K, Riboli, Elio, Vineis, Paolo, Vermeulen, Roel CH, Southey, Melissa C, Milne, Roger L, Clavel, Jacqueline, Topka, Sabine, Spinelli, John J, Kraft, Peter, Ennas, Maria Grazia, Summerfield, Geoffrey, Ferri, Giovanni M, Harris, Robert J, Miligi, Lucia, Pettitt, Andrew R, North, Kari E, Allsup, David J, Fraumeni, Joseph F, Bailey, James R, Offit, Kenneth, Pratt, Guy, Hjalgrim, Henrik, Pepper, Chris, Chanock, Stephen J, Fegan, Chris, Rosenquist, Richard, Sanjose, Silvia de, Carracedo, Angel, Dyer, Martin JS, Catovsky, Daniel, Campo, Elias, Cerhan, James R, Allan, James M, Rothman, Nathanial, Houlston, Richard, Slager, Susan, Law, P.J., Berndt, S.I., Speedy, H.E., Camp, N.J., Sava, G.P., Skibola, C.F., Holroyd, A., Joseph, V., Sunter, N.J., Nieters, A., Bea, S., Monnereau, A., Martin-Garcia, D., Goldin, L.R., Clot, G., Teras, L.R., Quintela, I., Birmann, B.M., Jayne, S., Cozen, W., Majid, A., Smedby, K.E., Lan, Q., Dearden, C., Brooks-Wilson, A.R., Hall, A.G., Purdue, M.P., Mainou-Fowler, T., Vajdic, C.M., Jackson, G.H., Cocco, P., Marr, H., Zhang, Y., Zheng, T., Giles, G.G., Lawrence, C., Call, T.G., Liebow, M., Melbye, M., Glimelius, B., Mansouri, L., Glenn, M., Curtin, K., Diver, W.R., Link, B.K., Conde, L., Bracci, P.M., Holly, E.A., Jackson, R.D., Tinker, L.F., Benavente, Y., Boffetta, P., Brennan, P., Maynadie, M., McKay, J., Albanes, D., Weinstein, S., Wang, Z., Caporaso, N.E., Morton, L.M., Severson, R.K., Riboli, E., Vineis, P., Vermeulen, R.C.H., Southey, M.C., Milne, R.L., Clavel, J., Topka, S., Spinelli, J.J., Kraft, P., Ennas, M.G., Summerfield, G., Ferri, G.M., Harris, R.J., Miligi, L., Pettitt, A.R., North, K.E., Allsup, D.J., Fraumeni, J.F., Jr., Bailey, J.R., Offit, K., Pratt, G., Hjalgrim, H., Pepper, C., Chanock, S.J., Fegan, C., Rosenquist, R., De Sanjose, S., Carracedo, A., Dyer, M.J.S., Catovsky, D., Campo, E., Cerhan, J.R., Allan, J.M., Rothman, N., Houlston, R., and Slager, S.

Subjects
Lymphocytic leukaemia
Abstract

Several chronic 14175 lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1,000 Genomes and UK10K data, totalling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P=5.04 × 10-13), 1q42.13 (rs41271473, P=1.06 × 10-10), 4q24 (rs71597109, P=1.37 × 10 -10), 4q35.1 (rs57214277, P=3.69 × 10-8), 6p21.31 (rs3800461, P=1.97 × 10-8), 11q23.2 (rs61904987, P=2.64 × 10-11), 18q21.1 (rs1036935, P=3.27 × 10-8), 19p13.3 (rs7254272, P=4.67 × 10-8) and 22q13.33 (rs140522, P=2.70 × 10-9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for the key determinants of B-cell development and immune response.

Published
2017

4. A genome-wide association study of marginal zone lymphoma shows association to the HLA region

Author

Vijai, Joseph, Wang, Zhaoming, Berndt, Sonja I, Skibola, Christine F, Slager, Susan L, de Sanjose, Silvia, Melbye, Mads, Glimelius, Bengt, Bracci, Paige M, Conde, Lucia, Birmann, Brenda M, Wang, Sophia S, Brooks-Wilson, Angela R, Lan, Qing, de Bakker, Paul IW, Vermeulen, Roel CH, Portlock, Carol, Ansell, Stephen M, Link, Brian K, Riby, Jacques, North, Kari E, Gu, Jian, Hjalgrim, Henrik, Cozen, Wendy, Becker, Nikolaus, Teras, Lauren R, Spinelli, John J, Turner, Jenny, Zhang, Yawei, Purdue, Mark P, Giles, Graham G, Kelly, Rachel S, Zeleniuch-Jacquotte, Anne, Ennas, Maria Grazia, Monnereau, Alain, Bertrand, Kimberly A, Albanes, Demetrius, Lightfoot, Tracy, Yeager, Meredith, Chung, Charles C, Burdett, Laurie, Hutchinson, Amy, Lawrence, Charles, Montalvan, Rebecca, Liang, Liming, Huang, Jinyan, Ma, Baoshan, Villano, Danylo J, Maria, Ann, Corines, Marina, Thomas, Tinu, Novak, Anne J, Dogan, Ahmet, Liebow, Mark, Thompson, Carrie A, Witzig, Thomas E, Habermann, Thomas M, Weiner, George J, Smith, Martyn T, Holly, Elizabeth A, Jackson, Rebecca D, Tinker, Lesley F, Ye, Yuanqing, Adami, Hans-Olov, Smedby, Karin E, De Roos, Anneclaire J, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Diver, W Ryan, Vajdic, Claire M, Armstrong, Bruce K, Kricker, Anne, Zheng, Tongzhang, Holford, Theodore R, Severi, Gianluca, Vineis, Paolo, Ferri, Giovanni M, Ricco, Rosalia, Miligi, Lucia, Clavel, Jacqueline, Giovannucci, Edward, Kraft, Peter, Virtamo, Jarmo, Smith, Alex, Kane, Eleanor, Roman, Eve, Chiu, Brian CH, Fraumeni, Joseph F, Wu, Xifeng, Cerhan, James R, Offit, Kenneth, and Chanock, Stephen J

Subjects
Membrane Glycoproteins, Genotype, Lymphoma, Butyrophilins, European Continental Ancestry Group, Human Genome, B-Cell, Computational Biology, Marginal Zone, Single Nucleotide, Hematology, White People, Major Histocompatibility Complex, Rare Diseases, Genetics, Humans, 2.1 Biological and endogenous factors, Polymorphism, Aetiology, Genome-Wide Association Study, Cancer
Abstract

Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.

Published
2015

5. Lung cancer risk among bricklayers in a pooled analysis of case-control studies

Author

Consonni, Dario, De Matteis, Sara, Pesatori, Angela C, Bertazzi, Pier Alberto, Olsson, Ann C, Kromhout, Hans, Peters, Susan, Vermeulen, Roel Ch, Pesch, Beate, Brüning, Thomas, Kendzia, Benjamin, Behrens, Thomas, Stücker, Isabelle, Guida, Florence, Wichmann, Heinz-Erich, Brüske, Irene, Landi, Maria Teresa, Caporaso, Neil E, Gustavsson, Per, Plato, Nils, Tse, Lap Ah, Yu, Ignatius Tak-Sun, Jöckel, Karl-Heinz, Ahrens, Wolfgang, Pohlabeln, Hermann, Merletti, Franco, Richiardi, Lorenzo, Simonato, Lorenzo, Forastiere, Francesco, Siemiatycki, Jack, Parent, Marie-Élise, Tardón, Adonina, Boffetta, Paolo, Zaridze, David, Chen, Ying, Field, John K, 't Mannetje, Andrea, Pearce, Neil, McLaughlin, John, Demers, Paul, Lissowska, Jolanta, Szeszenia-Dabrowska, Neonila, Bencko, Vladimir, Foretova, Lenka, Janout, Vladimir, Rudnai, Peter, Fabiánová, Eleonóra, Stanescu Dumitru, Rodica, Bueno-de-Mesquita, Bas, Schüz, Joachim, Straif, Kurt, Risk Assessment, Infection & Immunity, dIRAS RA-2, dIRAS RA-I&I RA, LS IRAS EEPI EXAS (Arb.hyg+bl.st.kar.), LS IRAS EEPI GRA (Gezh.risico-analyse), Consonni, D. and De Matteis, S. and Pesatori, A.C. and Bertazzi, P.A. and Olsson, A.C. and Kromhout, H. and Peters, S. and Vermeulen, R.C.H. and Pesch, B. and Brüning, T. and Kendzia, B. and Behrens, T. and Stücker, I. and Guida, F. and Wichmann, H.-E. and Brüske, I. and Landi, M.T. and Caporaso, N.E. and Gustavsson, P. and Plato, N. and Tse, L.A. and Yu, I.T.-S. and Jöckel, K.-H. and Ahrens, W. and Pohlabeln, H. and Merletti, F. and Richiardi, L. and Simonato, L. and Forastiere, F. and Siemiatycki, J. and Parent, M.-É. and Tardón, A. and Boffetta, P. and Zaridze, D. and Chen, Y. and Field, J.K. and Mannetje, A. and Pearce, N. and McLaughlin, J. and Demers, P. and Lissowska, J. and Szeszenia-Dabrowska, N. and Bencko, V. and Foretova, L. and Janout, V. and Rudnai, P. and Fabiánová, E. and Dumitru, R.S. and Bueno-De-Mesquita, H.B. and Schüz, J. and Straif, K., Courcelles, Michel, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Università degli Studi di Milano = University of Milan (UNIMI), Imperial College London, Centre International de Recherche contre le Cancer - International Agency for Research on Cancer (CIRC - IARC), Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), The Institute of Environmental Medicine [Stockholm] (IMM), Karolinska Institutet [Stockholm], Institute for Risk Assessment Sciences, Utrecht University [Utrecht], The University of Western Australia (UWA), Institute for Prevention and Occupational Medicine of the German Social Accident Insurance (IPA), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Deutsches Forschungszentrum für Gesundheit und Umwelt (GmbH), National Cancer Institute [Bethesda] (NCI-NIH), National Institutes of Health [Bethesda] (NIH), The Chinese University of Hong Kong [Hong Kong], University Hospital Essen, Leibniz Institute for Prevention Research and Epidemiology - BIPS, Leibniz Association, University of Bremen, Unit of Cancer Epidemiology, Université de Turin-CERMS and Centre for Oncologic Prevention, Università degli Studi di Padova = University of Padua (Unipd), Azienda Sanitaria Locale [ROMA] (ASL), Centre Hospitalier de l'Université de Montréal (CHUM), Université de Montréal (UdeM), Institut Armand Frappier (INRS-IAF), Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP), CIBER de Epidemiología y Salud Pública (CIBERESP), International Prevention Research Institute (IPRI), Icahn School of Medicine at Mount Sinai [New York] (MSSM), Institute of Carcinogenesis, Russian Cancer Research Centre, Keele University [Keele], University of Liverpool, London School of Hygiene and Tropical Medicine (LSHTM), Samuel Lunenfeld Research Institute, Mount Sinai Hospital [Toronto, Canada] (MSH), Cancer Care Ontario, The M Sklodowska-Curie Cancer Center and Institute of Oncology, The Nofer Institute of Occupational Medicine, Institute of Hygiene and Epidemiology, Charles University [Prague] (CU)-First Faculty of Medicine, Masaryk University [Brno] (MUNI), Department of Optics [Univ Palacký], Faculty of Science [Univ Palacký], Palacky University Olomouc-Palacky University Olomouc, National Institutes of Environmental Health Sciences, Regional Authority of Public Health [Slovaquia] (RAPH), Ministry of Health of the Slovak Republic [Slovaquia], Institute of Public Health, National Institute for Public Health and the Environment [Bilthoven] (RIVM), Grant sponsor: German Social Accident Insurance (DGUV), Grant number: FP 271, Grant sponsors: Canadian Institutes for Health Researchand Guzzo-SRC Chair in Environm ent and Cancer, National Cancer Institute of Canada, Canadian Cancer Society, Occupational Cancer ResearchCentre, Workplace Safety and Insuranc e Boar d, Canadian Cancer Society, and Cancer Care Ontario, Grant sponsor: European Commission’s INCO Copernicus program, Grant number: IC15-CT96-0313, Grant sponsor: European Union Nuclear Fission Safety Program, Grant number:F14P-CT96-0055, Grant sponsors: French Agency of Health Security (ANSES), Fondation de France, French National Research Agency (ANR),National Institute of Cancer (INCA), Fondation pour la Recherche Medicale, French Institute for Public Health Surveillance (InVS), Health Ministry (DGS), Organization for the Research on Cancer (ARC), and French Ministry of work, solidarity, and public function (DGT), Grant sponsor: Federal Ministry of Education, Science, Research, and Technology, Grant number: 01 HK 173/0), Grant sponsor: Federal Ministry of Science, Grant number:01 HK 546/8, Grant sponsor: Ministry of Labour and Social Affairs, Grant number: IIIb7-27/13, Grant sponsor: Research Grants Council of the Hong Kong Special Administrative Region, China, Grant number: CUHK4460/03M, Grant sponsors: Environmental Epidemiology Program of the Lombardy Region, INAIL, Italian Association for Cancer Research, Region Piedmont, Compagnia di San Paolo, Lazio Region, Health Research Council of New Zealand, New Zealand Department of Labour, Lottery Health Research, Cancer Society of New Zealand, Grant sponsor: Polish State Committee for Scientific Research, Grant number: SPUB-M-COPERNICUS/P-05/DZ-30/99/2000, Grant sponsors: Instituto Universitario de Oncologia, Universidad de Oviedo, Asturias, Fondo de Investigacion Sanitaria (FIS) and Ciber de Epidemiologia y Salud Publica (CIBERESP), Swedish Council for Work Life Research and Swedish Environmental Protection Agency, Dutch Ministry of Health, Welfare and Sports, National Institute of Public Health and the Environment, and Europe Against Cancer Program, Roy Castle Foundation, and Intramural Research Program of the National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, Maryland, Risk Assessment, Infection & Immunity, dIRAS RA-2, dIRAS RA-I&I RA, LS IRAS EEPI EXAS (Arb.hyg+bl.st.kar.), LS IRAS EEPI GRA (Gezh.risico-analyse), Università degli Studi di Milano [Milano] (UNIMI), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Universita degli Studi di Padova, Charles University and General University Hospital-First Faculty of Medicine, and Masaryk Memorial Cancer Institute and Medical Faculty of Masaryk University

Subjects
Male, Epidemiology, control studies, cancer risk, bricklayer, middle aged, occupation, CARCINOGENS, blue collar worker, POPULATION, comparative study, education.field_of_study, MESH: Middle Aged, risk assessment, WORKERS, MEN, MESH: Carcinoma, Squamous Cell, clinical trial, MESH: Follow-Up Studies, Prognosis, MESH: Case-Control Studies, 3. Good health, Occupational Diseases, [SDV] Life Sciences [q-bio], OCCUPATIONAL-EXPOSURE, hospital based case control study, Oncology, priority journal, risk factor, Adenocarcinoma, Carcinoma, Squamous Cell, case, Human, MESH: Occupational Diseases, medicine.medical_specialty, national cancer institute of, additional supporting information may, case–control studies, employment statu, MESH: Prognosis, Article, Follow-Up Studie, MESH: International Agencies, [SDV.CAN] Life Sciences [q-bio]/Cancer, carcinogen, adult, Humans, [SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health, research and guzzo-src chair, education, CRYSTALLINE SILICA DUST, fp 271, Science & Technology, MESH: Humans, Occupational health, MORTALITY, health care facility, Construction Industry, Case-control study, bricklayers, Odds ratio, case control study, medicine.disease, dguv, lung adenocarcinoma, major clinical study, Lung neoplasm, occupational hazard, MESH: Lung Neoplasms, Occupational Disease, occupational cancer, multicenter study, age, Relative risk, small cell lung cancer, Occupational medicine, MESH: Female, population research, Cancer Research, online version of this, [SDV]Life Sciences [q-bio], canada, Medizin, medicine.disease_cause, MESH: Occupational Exposure, grant number, Risk Factors, MESH: Risk Factors, Carcinoma, Small Cell, Medicine (all), international cooperation, grant sponsor, article, canadian institutes for health, MESH: Carcinoma, Small Cell, be found in the, MESH: Construction Industry, female, NORDIC COUNTRIES, International Agencie, canadian cancer society, epidemiology, grant sponsors, Gustavsson, in environment and cancer, Case-Control Studie, Life Sciences & Biomedicine, lifespan, prognosi, Population, UNITED-STATES, [SDV.CAN]Life Sciences [q-bio]/Cancer, lung neoplasms, Asbestos, smoking, building industry, occupational health, Internal medicine, Occupational Exposure, medicine, follow up, controlled study, occupational, Lung cancer, population based case control study, Plato, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, adenocarcinoma, business.industry, case-control studies, Risk Factor, Carcinoma, MESH: Adenocarcinoma, International Agencies, Small Cell, Confidence interval, MESH: Male, human tissue, Surgery, lung cancer, german social accident insurance, Squamous Cell, Bricklayers, Case-control studies, Lung neoplasms, Adenocarcinoma, Case-Control Studies, Female, Follow-Up Studies, Lung Neoplasms, Middle Aged, business, CONSTRUCTION-INDUSTRY, squamous cell lung carcinoma
Abstract

Bricklayers may be exposed to several lung carcinogens, including crystalline silica and asbestos. Previous studies that analyzed lung cancer risk among these workers had several study design limitations. We examined lung cancer risk among bricklayers within SYNERGY, a large international pooled analysis of case–control studies on lung cancer and the joint effects of occupational carcinogens. For men ever employed as bricklayers we estimated odds ratios (OR) and 95% confidence intervals (CI) adjusted for study center, age, lifetime smoking history and employment in occupations with exposures to known or suspected lung carcinogens. Among 15,608 cases and 18,531 controls, there were 695 cases and 469 controls who had ever worked as bricklayers (OR: 1.47; 95% CI: 1.28–1.68). In studies using population controls the OR was 1.55 (95% CI: 1.32–1.81, 540/349 cases/controls), while it was 1.24 (95% CI: 0.93–1.64, 155/120 cases/controls) in hospital-based studies. There was a clear positive trend with length of employment (p < 0.001). The relative risk was higher for squamous (OR: 1.68, 95% CI: 1.42–1.98, 309 cases) and small cell carcinomas (OR: 1.78, 95% CI: 1.44–2.20, 140 cases), than for adenocarcinoma (OR: 1.17, 95% CI: 0.95–1.43, 150 cases) (p-homogeneity: 0.0007). ORs were still elevated after additional adjustment for education and in analyses using blue collar workers as referents. This study provided robust evidence of increased lung cancer risk in bricklayers. Although non-causal explanations cannot be completely ruled out, the association is plausible in view of the potential for exposure to several carcinogens, notably crystalline silica and to a lesser extent asbestos. WHAT'S NEW?: In their work, bricklayers can be exposed to various airborne carcinogens, including crystalline silica and asbestos. Previous studies of cancer risk have not accounted for full employment history or smoking status, and failed to establish a firm relationship between bricklaying and lung cancer. In this study, the authors used data from the largest collection of case-control studies on lung cancer with complete occupational and smoking history existing today, the SYNERGY project. They found clear evidence that lung cancer risk increases in proportion to the length of time spent working as a bricklayer, paving the way for better protection and compensation for those in this occupation.

Published
2015
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6. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma

Author

Cerhan, James R, Berndt, Sonja I, Vijai, Joseph, Ghesquières, Hervé, McKay, James, Wang, Sophia S, Wang, Zhaoming, Yeager, Meredith, Conde, Lucia, de Bakker, Paul IW, Nieters, Alexandra, Cox, David, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Lan, Qing, Severi, Gianluca, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Teras, Lauren R, Purdue, Mark P, Vajdic, Claire M, Spinelli, John J, Giles, Graham G, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Weiner, George J, Veron, Amelie S, Zelenika, Diana, Tilly, Hervé, Haioun, Corinne, Molina, Thierry Jo, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Kricker, Anne, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Vermeulen, Roel CH, Boeing, Heiner, Tjonneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, and Birmann, Brenda M

Subjects
Likelihood Functions, Genotype, Lymphoma, Quantitative Trait Loci, Human Genome, Chromosome Mapping, Computational Biology, Single Nucleotide, Hematology, Biological Sciences, Diffuse, Medical and Health Sciences, White People, Rare Diseases, Genetic Loci, Large B-Cell, Genetics, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Polymorphism, Aetiology, Genome-Wide Association Study, Cancer, Developmental Biology
Abstract

Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.

Published
2014

7. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma

Author

Cerhan, James R, Berndt, Sonja I, Vijai, Joseph, Ghesquières, Hervé, McKay, James, Wang, Sophia S, Wang, Zhaoming, Yeager, Meredith, Conde, Lucia, de Bakker, Paul IW, Nieters, Alexandra, Cox, David, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Lan, Qing, Severi, Gianluca, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Teras, Lauren R, Purdue, Mark P, Vajdic, Claire M, Spinelli, John J, Giles, Graham G, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Weiner, George J, Veron, Amelie S, Zelenika, Diana, Tilly, Hervé, Haioun, Corinne, Molina, Thierry Jo, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Kricker, Anne, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Vermeulen, Roel CH, Boeing, Heiner, Tjonneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, and Birmann, Brenda M

Subjects
Likelihood Functions, Genotype, Lymphoma, Quantitative Trait Loci, European Continental Ancestry Group, Chromosome Mapping, Computational Biology, Single Nucleotide, Biological Sciences, Diffuse, Medical and Health Sciences, Genetic Loci, Large B-Cell, Humans, Genetic Predisposition to Disease, Polymorphism, Genome-Wide Association Study, Developmental Biology
Abstract

Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.

Published
2014

8. Genome-wide association study identifies five susceptibility loci for follicular lymphoma outside the HLA region

Author

Skibola, Christine F, Berndt, Sonja I, Vijai, Joseph, Conde, Lucia, Wang, Zhaoming, Yeager, Meredith, de Bakker, Paul IW, Birmann, Brenda M, Vajdic, Claire M, Foo, Jia-Nee, Bracci, Paige M, Vermeulen, Roel CH, Slager, Susan L, de Sanjose, Silvia, Wang, Sophia S, Linet, Martha S, Salles, Gilles, Lan, Qing, Severi, Gianluca, Hjalgrim, Henrik, Lightfoot, Tracy, Melbye, Mads, Gu, Jian, Ghesquières, Hervé, Link, Brian K, Morton, Lindsay M, Holly, Elizabeth A, Smith, Alex, Tinker, Lesley F, Teras, Lauren R, Kricker, Anne, Becker, Nikolaus, Purdue, Mark P, Spinelli, John J, Zhang, Yawei, Giles, Graham G, Vineis, Paolo, Monnereau, Alain, Bertrand, Kimberly A, Albanes, Demetrius, Zeleniuch-Jacquotte, Anne, Gabbas, Attilio, Chung, Charles C, Burdett, Laurie, Hutchinson, Amy, Lawrence, Charles, Montalvan, Rebecca, Liang, Liming, Huang, Jinyan, Ma, Baoshan, Liu, Jianjun, Adami, Hans-Olov, Glimelius, Bengt, Ye, Yuanqing, Nowakowski, Grzegorz S, Dogan, Ahmet, Thompson, Carrie A, Habermann, Thomas M, Novak, Anne J, Liebow, Mark, Witzig, Thomas E, Weiner, George J, Schenk, Maryjean, Hartge, Patricia, De Roos, Anneclaire J, Cozen, Wendy, Zhi, Degui, Akers, Nicholas K, Riby, Jacques, Smith, Martyn T, Lacher, Mortimer, Villano, Danylo J, Maria, Ann, Roman, Eve, Kane, Eleanor, Jackson, Rebecca D, North, Kari E, Diver, W Ryan, Turner, Jenny, Armstrong, Bruce K, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, McKay, James, Brooks-Wilson, Angela R, Zheng, Tongzhang, Holford, Theodore R, Chamosa, Saioa, Kaaks, Rudolph, Kelly, Rachel S, Ohlsson, Bodil, Travis, Ruth C, Weiderpass, Elisabete, Clavel, Jacqueline, Giovannucci, Edward, Kraft, Peter, and Virtamo, Jarmo

Subjects
Lymphoma, Medical and Health Sciences, Chromosomes, Rare Diseases, HLA Antigens, Clinical Research, Genetics, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Polymorphism, Aetiology, Alleles, Cancer, Genetics & Heredity, Tumor, Human Genome, Follicular, Single Nucleotide, Hematology, Biological Sciences, Haplotypes, Case-Control Studies, Biomarkers, Human, Genome-Wide Association Study
Abstract

Genome-wide association studies (GWASs) of follicular lymphoma (FL) have previously identified human leukocyte antigen (HLA) gene variants. To identify additional FL susceptibility loci, we conducted a large-scale two-stage GWAS in 4,523 case subjects and 13,344 control subjects of European ancestry. Five non-HLA loci were associated with FL risk: 11q23.3 (rs4938573, p = 5.79 × 10(-20)) near CXCR5; 11q24.3 (rs4937362, p = 6.76 × 10(-11)) near ETS1; 3q28 (rs6444305, p = 1.10 × 10(-10)) in LPP; 18q21.33 (rs17749561, p = 8.28 × 10(-10)) near BCL2; and 8q24.21 (rs13254990, p = 1.06 × 10(-8)) near PVT1. In an analysis of the HLA region, we identified four linked HLA-DRβ1 multiallelic amino acids at positions 11, 13, 28, and 30 that were associated with FL risk (pomnibus = 4.20 × 10(-67) to 2.67 × 10(-70)). Additional independent signals included rs17203612 in HLA class II (odds ratio [OR(per-allele)] = 1.44; p = 4.59 × 10(-16)) and rs3130437 in HLA class I (OR(per-allele) = 1.23; p = 8.23 × 10(-9)). Our findings further expand the number of loci associated with FL and provide evidence that multiple common variants outside the HLA region make a significant contribution to FL risk.

Published
2014

9. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia

Author

Berndt, Sonja I, Skibola, Christine F, Joseph, Vijai, Camp, Nicola J, Nieters, Alexandra, Wang, Zhaoming, Cozen, Wendy, Monnereau, Alain, Wang, Sophia S, Kelly, Rachel S, Lan, Qing, Teras, Lauren R, Chatterjee, Nilanjan, Chung, Charles C, Yeager, Meredith, Brooks-Wilson, Angela R, Hartge, Patricia, Purdue, Mark P, Birmann, Brenda M, Armstrong, Bruce K, Cocco, Pierluigi, Zhang, Yawei, Severi, Gianluca, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Burdette, Laurie, Yuenger, Jeffrey, Hutchinson, Amy, Jacobs, Kevin B, Call, Timothy G, Shanafelt, Tait D, Novak, Anne J, Kay, Neil E, Liebow, Mark, Wang, Alice H, Smedby, Karin E, Adami, Hans-Olov, Melbye, Mads, Glimelius, Bengt, Chang, Ellen T, Glenn, Martha, Curtin, Karen, Cannon-Albright, Lisa A, Jones, Brandt, Diver, W Ryan, Link, Brian K, Weiner, George J, Conde, Lucia, Bracci, Paige M, Riby, Jacques, Holly, Elizabeth A, Smith, Martyn T, Jackson, Rebecca D, Tinker, Lesley F, Benavente, Yolanda, Becker, Nikolaus, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Rabe, Kari G, Achenbach, Sara J, Vachon, Celine M, Goldin, Lynn R, Strom, Sara S, Lanasa, Mark C, Spector, Logan G, Leis, Jose F, Cunningham, Julie M, Weinberg, J Brice, Morrison, Vicki A, Caporaso, Neil E, Norman, Aaron D, Linet, Martha S, De Roos, Anneclaire J, Morton, Lindsay M, Severson, Richard K, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Masala, Giovanna, Weiderpass, Elisabete, Chirlaque, María-Dolores, Vermeulen, Roel CH, Travis, Ruth C, Giles, Graham G, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Clavel, Jacqueline, Zheng, Tongzhang, Holford, Theodore R, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Spinelli, John J, and Bertrand, Kimberly A

Subjects
Risk, Leukemia, B-Cell, Single Nucleotide, Biological Sciences, Medical and Health Sciences, Chromosomes, Recombination, Linkage Disequilibrium, Lymphocytic, Genetic, Genetic Loci, Case-Control Studies, Pair 2, Humans, Genetic Predisposition to Disease, Polymorphism, Chronic, Human, Genome-Wide Association Study, Developmental Biology
Abstract

Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P=1.22×10(-14)), 18q21.33 (BCL2, P=7.76×10(-11)), 11p15.5 (C11orf21, P=2.15×10(-10)), 4q25 (LEF1, P=4.24×10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P=2.50×10(-9)), 9p21.3 (CDKN2B-AS1, P=1.27×10(-8)), 18q21.32 (PMAIP1, P=2.51×10(-8)), 15q15.1 (BMF, P=2.71×10(-10)) and 2p22.2 (QPCT, P=1.68×10(-8)), as well as an independent signal at an established locus (2q13, ACOXL, P=2.08×10(-18)). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P=5.40×10(-8)) and 5p15.33 (TERT, P=1.92×10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.

Published
2013

10. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia

Author

Berndt, Sonja I, Skibola, Christine F, Joseph, Vijai, Camp, Nicola J, Nieters, Alexandra, Wang, Zhaoming, Cozen, Wendy, Monnereau, Alain, Wang, Sophia S, Kelly, Rachel S, Lan, Qing, Teras, Lauren R, Chatterjee, Nilanjan, Chung, Charles C, Yeager, Meredith, Brooks-Wilson, Angela R, Hartge, Patricia, Purdue, Mark P, Birmann, Brenda M, Armstrong, Bruce K, Cocco, Pierluigi, Zhang, Yawei, Severi, Gianluca, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Burdette, Laurie, Yuenger, Jeffrey, Hutchinson, Amy, Jacobs, Kevin B, Call, Timothy G, Shanafelt, Tait D, Novak, Anne J, Kay, Neil E, Liebow, Mark, Wang, Alice H, Smedby, Karin E, Adami, Hans-Olov, Melbye, Mads, Glimelius, Bengt, Chang, Ellen T, Glenn, Martha, Curtin, Karen, Cannon-Albright, Lisa A, Jones, Brandt, Diver, W Ryan, Link, Brian K, Weiner, George J, Conde, Lucia, Bracci, Paige M, Riby, Jacques, Holly, Elizabeth A, Smith, Martyn T, Jackson, Rebecca D, Tinker, Lesley F, Benavente, Yolanda, Becker, Nikolaus, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Rabe, Kari G, Achenbach, Sara J, Vachon, Celine M, Goldin, Lynn R, Strom, Sara S, Lanasa, Mark C, Spector, Logan G, Leis, Jose F, Cunningham, Julie M, Weinberg, J Brice, Morrison, Vicki A, Caporaso, Neil E, Norman, Aaron D, Linet, Martha S, De Roos, Anneclaire J, Morton, Lindsay M, Severson, Richard K, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Masala, Giovanna, Weiderpass, Elisabete, Chirlaque, María-Dolores, Vermeulen, Roel CH, Travis, Ruth C, Giles, Graham G, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Clavel, Jacqueline, Zheng, Tongzhang, Holford, Theodore R, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Spinelli, John J, and Bertrand, Kimberly A

Subjects
Risk, Leukemia, B-Cell, Single Nucleotide, Biological Sciences, Medical and Health Sciences, Chromosomes, Recombination, Linkage Disequilibrium, Lymphocytic, Genetic, Genetic Loci, Case-Control Studies, Pair 2, Humans, Genetic Predisposition to Disease, Polymorphism, Chronic, Human, Genome-Wide Association Study, Cancer, Developmental Biology
Abstract

Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P=1.22×10(-14)), 18q21.33 (BCL2, P=7.76×10(-11)), 11p15.5 (C11orf21, P=2.15×10(-10)), 4q25 (LEF1, P=4.24×10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P=2.50×10(-9)), 9p21.3 (CDKN2B-AS1, P=1.27×10(-8)), 18q21.32 (PMAIP1, P=2.51×10(-8)), 15q15.1 (BMF, P=2.71×10(-10)) and 2p22.2 (QPCT, P=1.68×10(-8)), as well as an independent signal at an established locus (2q13, ACOXL, P=2.08×10(-18)). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P=5.40×10(-8)) and 5p15.33 (TERT, P=1.92×10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.

Published
2013

11. Diabetes and the risk of non-Hodgkin's lymphoma and multiple myeloma in the European Prospective Investigation into Cancer and Nutrition

Author

Khan, Aneire E, Gallo, Valentina, Linseisen, Jakob, Kaaks, Rudolf, Rohrmann, Sabine, Raaschou-Nielsen, Ole, Tjønneland, Anne, Johnsen, Hans E, Overvad, Kim, Bergmann, Manuela M, Boeing, Heiner, Benetou, Vasiliki, Psaltopoulou, Theodora, Trichopoulou, Antonia, Masala, Giovanna, Mattiello, Amalia, Grioni, Sara, Tumino, Rosario, Vermeulen, Roel CH, Peeters, Petra HM, Bueno-de-Mesquita, H Bas, Ros, Martine M, Lund, Eiliv, Ardanaz, Eva, Chirlaque, María-Dolores, Jakszyn, Paula, Larrañaga, Nerea, Losada, Adamina, Becker, Nikolaus, Nieters, Alexandra, Martínez-García, Carmen, Agren, Asa, Hallmans, Göran, Berglund, Göran, Manjer, Jonas, Allen, Naomi E, Key, Timothy J, Bingham, Sheila, Khaw, Kay Tee, Slimani, Nadia, Ferrari, Pietro, Boffetta, Paolo, Norat, Teresa, Vineis, Paolo, Riboli, Elio, and EPIC Group

Subjects
immune system diseases, hemic and lymphatic diseases
Abstract

BACKGROUND: Non-Hodgkin's lymphomas are a heterogeneous group of neoplasms arising from the lymphopoietic system including a wide range of subtypes of either B-cell or T-cell lymphomas. The few established risk factors for the development of these neoplasms include viral infections and immunological abnormalities, but their etiology remains largely unknown. Evidence suggests that certain medical conditions may be linked, through immunosuppression, to the risk of non-Hodgkin's lymphoma. Multiple myeloma is a neoplasm of plasma cells that accounts for approximately 15% of lymphopoietic cancers. Increases in the incidence of non-Hodgkin's lymphoma and multiple myeloma in the past implicate environmental factors as potential causal agents. DESIGN AND METHODS: In the European Prospective Investigation into Cancer and Nutrition (EPIC), 1,213 histologically confirmed incident cases of non-Hodgkin's lymphoma and multiple myeloma (594 men; 619 women) were identified during a follow-up of 8.5 years. Cox proportional hazard models were used to explore the association between self-reported diabetes, diagnosed after 30 years of age, and the risk of non-Hodgkin's lymphoma overall and multiple myeloma and various lymphoma subtypes. RESULTS: We found no association between a personal history of diabetes and the risk of non-Hodgkin's lymphoma overall in men (HR: 1.28, 95% CI: 0.89-1.84), in women (HR: 0.71, 95% CI: 0.41- 1.24), or in men and women combined (HR: 1.09, 95% CI: 0.80-1.47). Among the B-non-Hodgkin's lymphoma subtypes, we observed a statistically significant increased risk of B-cell chronic lymphocytic leukemia (HR: 2.0, 95% CI: 1.04-3.86) in men, but not in women (HR: 1.07, 95% CI: 0.33-3.43). CONCLUSIONS: This prospective study did not provide evidence for a role of self-reported diabetes in the etiology of non-Hodgkin's lymphoma overall or multiple myeloma. We found an increased risk of B-cell chronic lymphocytic leukemia among men with diabetes, but not among women. We hypothesize that diabetes may not play a causal role in the etiology of B-cell chronic lymphocytic leukemia, though the underlying pathogenic mechanisms of both disorders may include shared genetic, host and/or environmental susceptibility factors.

Published
2008

12. Association of Selenoprotein and Selenium Pathway Genotypes with Risk of Colorectal Cancer and Interaction with Selenium Status

Author

Fedirko, Veronika, Jenab, Mazda, Méplan, Catherine, Jones, Jeb S, Zhu, Wanzhe, Schomburg, Lutz, Siddiq, Afshan, Hybsier, Sandra, Overvad, Kim, Tjønneland, Anne, Omichessan, Hanane, Perduca, Vittorio, Boutron-Ruault, Marie-Christine, Kühn, Tilman, Katzke, Verena, Aleksandrova, Krasimira, Trichopoulou, Antonia, Karakatsani, Anna, Kotanidou, Anastasia, Tumino, Rosario, Panico, Salvatore, Masala, Giovanna, Agnoli, Claudia, Naccarati, Alessio, Bueno-De-Mesquita, Bas, Vermeulen, Roel CH, Weiderpass, Elisabete, Skeie, Guri, Nøst, Therese Haugdahl, Lujan-Barroso, Leila, Quirós, J Ramón, Huerta, José María, Rodríguez-Barranco, Miguel, Barricarte, Aurelio, Gylling, Björn, Harlid, Sophia, Bradbury, Kathryn E, Wareham, Nick, Khaw, Kay-Tee, Gunter, Marc, Murphy, Neil, Freisling, Heinz, Tsilidis, Kostas, Aune, Dagfinn, Riboli, Elio, Hesketh, John E, and Hughes, David J

Subjects
Adult, Male, genetic epidemiology, Genotype, selenoprotein P, prospective cohort, Nutritional Status, selenoprotein gene variation, Polymorphism, Single Nucleotide, Cohort Studies, Selenium, Humans, Genetic Predisposition to Disease, Prospective Studies, Selenoproteins, Aged, integumentary system, colorectal cancer risk, biomarkers, colorectal neoplasms, Middle Aged, 3. Good health, selenium pathway, Gene Expression Regulation, selenium status, Female
Abstract

Selenoprotein genetic variations and suboptimal selenium (Se) levels may contribute to the risk of colorectal cancer (CRC) development. We examined the association between CRC risk and genotype for single nucleotide polymorphisms (SNPs) in selenoprotein and Se metabolic pathway genes. Illumina Goldengate assays were designed and resulted in the genotyping of 1040 variants in 154 genes from 1420 cases and 1421 controls within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Multivariable logistic regression revealed an association of 144 individual SNPs from 63 Se pathway genes with CRC risk. However, regarding the selenoprotein genes, only TXNRD1 rs11111979 retained borderline statistical significance after adjustment for correlated tests (PACT = 0.10; PACT significance threshold was P < 0.1). SNPs in Wingless/Integrated (Wnt) and Transforming growth factor (TGF) beta-signaling genes (FRZB, SMAD3, SMAD7) from pathways affected by Se intake were also associated with CRC risk after multiple testing adjustments. Interactions with Se status (using existing serum Se and Selenoprotein P data) were tested at the SNP, gene, and pathway levels. Pathway analyses using the modified Adaptive Rank Truncated Product method suggested that genes and gene x Se status interactions in antioxidant, apoptosis, and TGF-beta signaling pathways may be associated with CRC risk. This study suggests that SNPs in the Se pathway alone or in combination with suboptimal Se status may contribute to CRC development.

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