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1. Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes

Author

Din, Lennox, Sheikh, Mohammad, Kosaraju, Nikitha, Smedby, Karin Ekstrom, Bernatsky, Sasha, Berndt, Sonja I, Skibola, Christine F, Nieters, Alexandra, Wang, Sophia, McKay, James D, Cocco, Pierluigi, Maynadié, Marc, Foretová, Lenka, Staines, Anthony, Mack, Thomas M, de Sanjosé, Silvia, Vyse, Timothy J, Padyukov, Leonid, Monnereau, Alain, Arslan, Alan A, Moore, Amy, Brooks‐Wilson, Angela R, Novak, Anne J, Glimelius, Bengt, Birmann, Brenda M, Link, Brian K, Stewart, Carolyn, Vajdic, Claire M, Haioun, Corinne, Magnani, Corrado, Conti, David V, Cox, David G, Casabonne, Delphine, Albanes, Demetrius, Kane, Eleanor, Roman, Eve, Muzi, Giacomo, Salles, Gilles, Giles, Graham G, Adami, Hans‐Olov, Ghesquières, Hervé, De Vivo, Immaculata, Clavel, Jacqueline, Cerhan, James R, Spinelli, John J, Hofmann, Jonathan, Vijai, Joseph, Curtin, Karen, Costenbader, Karen H, Onel, Kenan, Offit, Kenneth, Teras, Lauren R, Morton, Lindsay, Conde, Lucia, Miligi, Lucia, Melbye, Mads, Ennas, Maria Grazia, Liebow, Mark, Purdue, Mark P, Glenn, Martha, Southey, Melissa C, Din, Morris, Rothman, Nathaniel, Camp, Nicola J, Doo, Nicole Wong, Becker, Nikolaus, Pradhan, Nisha, Bracci, Paige M, Boffetta, Paolo, Vineis, Paolo, Brennan, Paul, Kraft, Peter, Lan, Qing, Severson, Richard K, Vermeulen, Roel CH, Milne, Roger L, Kaaks, Rudolph, Travis, Ruth C, Weinstein, Stephanie J, Chanock, Stephen J, Ansell, Stephen M, Slager, Susan L, Zheng, Tongzhang, Zhang, Yawei, Benavente, Yolanda, Taub, Zachary, Madireddy, Lohith, Gourraud, Pierre‐Antoine, Oksenberg, Jorge R, Cozen, Wendy, Hjalgrim, Henrik, and Khankhanian, Pouya

Subjects
Biological Sciences, Genetics, Lymphoma, Arthritis, Neurodegenerative, Brain Disorders, Autoimmune Disease, Cancer, Human Genome, Rare Diseases, Hematology, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Alleles, Autoimmune Diseases, Female, Genetic Predisposition to Disease, HLA Antigens, Humans, Lymphoma, Non-Hodgkin, Male, Middle Aged, Multifactorial Inheritance, Polymorphism, Single Nucleotide, Risk Factors, autoimmune disease, genome-wide association study, meta-analysis, non-Hodgkin lymphoma, Public Health and Health Services, Epidemiology
Abstract

Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.

Published
2019

2. Evaluating the mechanistic evidence and key data gaps in assessing the potential carcinogenicity of carbon nanotubes and nanofibers in humans

Author

Kuempel, Eileen D, Jaurand, Marie-Claude, Møller, Peter, Morimoto, Yasuo, Kobayashi, Norihiro, Pinkerton, Kent E, Sargent, Linda M, Vermeulen, Roel CH, Fubini, Bice, and Kane, Agnes B

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Prevention, Bioengineering, Cancer, Nanotechnology, Animals, Carcinogenicity Tests, Humans, Nanofibers, Nanotubes, Carbon, Cancer mechanisms, carbon nanofibers, carbon nanotubes, cell proliferation, fibrosis, genotoxicity, inflammation, lung cancer, mesothelioma, particle retention, pulmonary, translocation, Pharmacology and Pharmaceutical Sciences, Toxicology, Pharmacology and pharmaceutical sciences
Abstract

In an evaluation of carbon nanotubes (CNTs) for the IARC Monograph 111, the Mechanisms Subgroup was tasked with assessing the strength of evidence on the potential carcinogenicity of CNTs in humans. The mechanistic evidence was considered to be not strong enough to alter the evaluations based on the animal data. In this paper, we provide an extended, in-depth examination of the in vivo and in vitro experimental studies according to current hypotheses on the carcinogenicity of inhaled particles and fibers. We cite additional studies of CNTs that were not available at the time of the IARC meeting in October 2014, and extend our evaluation to include carbon nanofibers (CNFs). Finally, we identify key data gaps and suggest research needs to reduce uncertainty. The focus of this review is on the cancer risk to workers exposed to airborne CNT or CNF during the production and use of these materials. The findings of this review, in general, affirm those of the original evaluation on the inadequate or limited evidence of carcinogenicity for most types of CNTs and CNFs at this time, and possible carcinogenicity of one type of CNT (MWCNT-7). The key evidence gaps to be filled by research include: investigation of possible associations between in vitro and early-stage in vivo events that may be predictive of lung cancer or mesothelioma, and systematic analysis of dose-response relationships across materials, including evaluation of the influence of physico-chemical properties and experimental factors on the observation of nonmalignant and malignant endpoints.

Published
2017

3. BMI and breast cancer risk around age at menopause

Author

Von Holle, Ann, Adami, Hans-Olov, Baglietto, Laura, Berrington, Amy, Bertrand, Kimberly A, Blot, William, Chen, Yu, DeHart, Jessica Clague, Dossus, Laure, Eliassen, A Heather, Fournier, Agnes, Garcia-Closas, Montse, Giles, Graham, Guevara, Marcela, Hankinson, Susan E, Heath, Alicia, Jones, Michael E, Joshu, Corinne E, Kaaks, Rudolf, Kirsh, Victoria A, Kitahara, Cari M, Koh, Woon-Puay, Linet, Martha S, Park, Hannah Lui, Masala, Giovanna, Mellemkjaer, Lene, Milne, Roger L, O'Brien, Katie M, Palmer, Julie R, Riboli, Elio, Rohan, Thomas E, Shrubsole, Martha J, Sund, Malin, Tamimi, Rulla, Tin Tin, Sandar, Visvanathan, Kala, Vermeulen, Roel Ch, Weiderpass, Elisabete, Willett, Walter C, Yuan, Jian-Min, Zeleniuch-Jacquotte, Anne, Nichols, Hazel B, Sandler, Dale P, Swerdlow, Anthony J, Schoemaker, Minouk J, Weinberg, Clarice R, Von Holle, Ann, Adami, Hans-Olov, Baglietto, Laura, Berrington, Amy, Bertrand, Kimberly A, Blot, William, Chen, Yu, DeHart, Jessica Clague, Dossus, Laure, Eliassen, A Heather, Fournier, Agnes, Garcia-Closas, Montse, Giles, Graham, Guevara, Marcela, Hankinson, Susan E, Heath, Alicia, Jones, Michael E, Joshu, Corinne E, Kaaks, Rudolf, Kirsh, Victoria A, Kitahara, Cari M, Koh, Woon-Puay, Linet, Martha S, Park, Hannah Lui, Masala, Giovanna, Mellemkjaer, Lene, Milne, Roger L, O'Brien, Katie M, Palmer, Julie R, Riboli, Elio, Rohan, Thomas E, Shrubsole, Martha J, Sund, Malin, Tamimi, Rulla, Tin Tin, Sandar, Visvanathan, Kala, Vermeulen, Roel Ch, Weiderpass, Elisabete, Willett, Walter C, Yuan, Jian-Min, Zeleniuch-Jacquotte, Anne, Nichols, Hazel B, Sandler, Dale P, Swerdlow, Anthony J, Schoemaker, Minouk J, and Weinberg, Clarice R

Abstract

BACKGROUND: A high body mass index (BMI, kg/m 2) is associated with decreased risk of breast cancer before menopause, but increased risk after menopause. Exactly when this reversal occurs in relation to menopause is unclear. Locating that change point could provide insight into the role of adiposity in breast cancer etiology. METHODS: We examined the association between BMI and breast cancer risk in the Premenopausal Breast Cancer Collaborative Group, from age 45 up to breast cancer diagnosis, loss to follow-up, death, or age 55, whichever came first. Analyses included 609,880 women in 16 prospective studies, including 9956 who developed breast cancer before age 55. We fitted three BMI hazard ratio (HR) models over age-time: constant, linear, or nonlinear (via splines), applying piecewise exponential additive mixed models, with age as the primary time scale. We divided person-time into four strata: premenopause; postmenopause due to natural menopause; postmenopause because of interventional loss of ovarian function (bilateral oophorectomy (BO) or chemotherapy); postmenopause due to hysterectomy without BO. Sensitivity analyses included stratifying by BMI in young adulthood, or excluding women using menopausal hormone therapy.RESULTS: The constant BMI HR model provided the best fit for all four menopausal status groups. Under this model, the estimated association between a five-unit increment in BMI and breast cancer risk was HR=0.87 (95% CI: 0.85, 0.89) before menopause, HR=1.00 (95% CI: 0.96, 1.04) after natural menopause, HR=0.99 (95% CI: 0.93, 1.05) after interventional loss of ovarian function, and HR=0.88 (95% CI: 0.76, 1.02) after hysterectomy without BO.CONCLUSION: The BMI breast cancer HRs remained less than or near one during the 45-55 year age range indicating that the transition to a positive association between BMI and risk occurs after age 55.

Published
2024

4. BMI and breast cancer risk around age at menopause

Author

IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Von Holle, Ann, Adami, Hans-Olov, Baglietto, Laura, Berrington, Amy, Bertrand, Kimberly A, Blot, William, Chen, Yu, DeHart, Jessica Clague, Dossus, Laure, Eliassen, A Heather, Fournier, Agnes, Garcia-Closas, Montse, Giles, Graham, Guevara, Marcela, Hankinson, Susan E, Heath, Alicia, Jones, Michael E, Joshu, Corinne E, Kaaks, Rudolf, Kirsh, Victoria A, Kitahara, Cari M, Koh, Woon-Puay, Linet, Martha S, Park, Hannah Lui, Masala, Giovanna, Mellemkjaer, Lene, Milne, Roger L, O'Brien, Katie M, Palmer, Julie R, Riboli, Elio, Rohan, Thomas E, Shrubsole, Martha J, Sund, Malin, Tamimi, Rulla, Tin Tin, Sandar, Visvanathan, Kala, Vermeulen, Roel Ch, Weiderpass, Elisabete, Willett, Walter C, Yuan, Jian-Min, Zeleniuch-Jacquotte, Anne, Nichols, Hazel B, Sandler, Dale P, Swerdlow, Anthony J, Schoemaker, Minouk J, Weinberg, Clarice R, IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Von Holle, Ann, Adami, Hans-Olov, Baglietto, Laura, Berrington, Amy, Bertrand, Kimberly A, Blot, William, Chen, Yu, DeHart, Jessica Clague, Dossus, Laure, Eliassen, A Heather, Fournier, Agnes, Garcia-Closas, Montse, Giles, Graham, Guevara, Marcela, Hankinson, Susan E, Heath, Alicia, Jones, Michael E, Joshu, Corinne E, Kaaks, Rudolf, Kirsh, Victoria A, Kitahara, Cari M, Koh, Woon-Puay, Linet, Martha S, Park, Hannah Lui, Masala, Giovanna, Mellemkjaer, Lene, Milne, Roger L, O'Brien, Katie M, Palmer, Julie R, Riboli, Elio, Rohan, Thomas E, Shrubsole, Martha J, Sund, Malin, Tamimi, Rulla, Tin Tin, Sandar, Visvanathan, Kala, Vermeulen, Roel Ch, Weiderpass, Elisabete, Willett, Walter C, Yuan, Jian-Min, Zeleniuch-Jacquotte, Anne, Nichols, Hazel B, Sandler, Dale P, Swerdlow, Anthony J, Schoemaker, Minouk J, and Weinberg, Clarice R

Published
2024

5. Genetically predicted longer telomere length is associated with increased risk of B-cell lymphoma subtypes

Author

Machiela, Mitchell J, Lan, Qing, Slager, Susan L, Vermeulen, Roel CH, Teras, Lauren R, Camp, Nicola J, Cerhan, James R, Spinelli, John J, Wang, Sophia S, Nieters, Alexandra, Vijai, Joseph, Yeager, Meredith, Wang, Zhaoming, Ghesquières, Hervé, McKay, James, Conde, Lucia, de Bakker, Paul IW, Cox, David G, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Giles, Graham G, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Purdue, Mark P, Vajdic, Claire M, 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, Tilly, Hervé, Haioun, Corinne, Molina, Thierry J, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Roos, Göran, 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, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Boeing, Heiner, Tjønneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, De Vivo, Immaculata, Giovannucci, Edward, Kraft, Peter, and Huang, Jinyan

Subjects
Clinical Research, Rare Diseases, Genetics, Cancer, Hematology, Lymphoma, Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Female, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Lymphoma, B-Cell, Male, Middle Aged, Prospective Studies, Telomere, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Evidence from a small number of studies suggests that longer telomere length measured in peripheral leukocytes is associated with an increased risk of non-Hodgkin lymphoma (NHL). However, these studies may be biased by reverse causation, confounded by unmeasured environmental exposures and might miss time points for which prospective telomere measurement would best reveal a relationship between telomere length and NHL risk. We performed an analysis of genetically inferred telomere length and NHL risk in a study of 10 102 NHL cases of the four most common B-cell histologic types and 9562 controls using a genetic risk score (GRS) comprising nine telomere length-associated single-nucleotide polymorphisms. This approach uses existing genotype data and estimates telomere length by weighing the number of telomere length-associated variant alleles an individual carries with the published change in kb of telomere length. The analysis of the telomere length GRS resulted in an association between longer telomere length and increased NHL risk [four B-cell histologic types combined; odds ratio (OR) = 1.49, 95% CI 1.22-1.82,P-value = 8.5 × 10(-5)]. Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL subtype contributing to this association (OR = 2.60, 95% CI 1.93-3.51,P-value = 4.0 × 10(-10)). Significant interactions were observed across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the follicular lymphoma subtype. Our results indicate that a genetic background that favors longer telomere length may increase NHL risk, particularly risk of CLL/SLL, and are consistent with earlier studies relating longer telomere length with increased NHL risk.

Published
2016

6. 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
Humans, Membrane Glycoproteins, Computational Biology, Major Histocompatibility Complex, Genotype, Polymorphism, Single Nucleotide, European Continental Ancestry Group, Lymphoma, B-Cell, Marginal Zone, Genome-Wide Association Study, Butyrophilins, Polymorphism, Single Nucleotide, Lymphoma, B-Cell, Marginal Zone
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

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
Human Genome, Rare Diseases, Genetics, Cancer, Hematology, Lymphoma, Aetiology, 2.1 Biological and endogenous factors, Chromosome Mapping, Computational Biology, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Likelihood Functions, Lymphoma, Large B-Cell, Diffuse, Polymorphism, Single Nucleotide, Quantitative Trait Loci, White People, Biological Sciences, Medical and Health Sciences, 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
Hematology, Cancer, Clinical Research, Human Genome, Lymphoma, Genetics, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Alleles, Biomarkers, Tumor, Case-Control Studies, Chromosomes, Human, Genetic Predisposition to Disease, Genome-Wide Association Study, HLA Antigens, Haplotypes, Humans, Lymphoma, Follicular, Polymorphism, Single Nucleotide, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
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
Cancer, Case-Control Studies, Chromosomes, Human, Pair 2, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Recombination, Genetic, Risk, Biological Sciences, Medical and Health Sciences, 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. 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

11. 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

12. Blood pressure and risk of cancer in the European Prospective Investigation into Cancer and Nutrition

Author

Christakoudi, Sofia, Kakourou, Artemisia, Markozannes, Georgios, Tzoulaki, Ioanna, Weiderpass, Elisabete, Brennan, Paul, Gunter, Marc, Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjonneland, Anne, Boutron-Ruault, Marie-Christine, Madika, Anne-Laure, Severi, Gianluca, Katzke, Verena, Kuehn, Tilman, Bergmann, Manuela M., Boeing, Heiner, Karakatsani, Anna, Martimianaki, Georgia, Thriskos, Paschalis, Masala, Giovanna, Sieri, Sabina, Panico, Salvatore, Tumino, Rosario, Ricceri, Fulvio, Agudo, Antonio, Redondo-Sanchez, Daniel, Colorado-Yohar, Sandra M., Mokoroa, Olatz, Melander, Ole, Stocks, Tanja, Häggström, Christel, Harlid, Sophia, Bueno-de-Mesquita, Bas, van Gils, Carla H., Vermeulen, Roel Ch, Khaw, Kay-Tee, Wareham, Nicholas J., Tong, Tammy Y. N., Freisling, Heinz, Johansson, Mattias, Lennon, Hannah, AUne, Dagfinn, Ribolil, Elio, Trichopoulos, Dimitrios, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Christakoudi, Sofia, Kakourou, Artemisia, Markozannes, Georgios, Tzoulaki, Ioanna, Weiderpass, Elisabete, Brennan, Paul, Gunter, Marc, Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjonneland, Anne, Boutron-Ruault, Marie-Christine, Madika, Anne-Laure, Severi, Gianluca, Katzke, Verena, Kuehn, Tilman, Bergmann, Manuela M., Boeing, Heiner, Karakatsani, Anna, Martimianaki, Georgia, Thriskos, Paschalis, Masala, Giovanna, Sieri, Sabina, Panico, Salvatore, Tumino, Rosario, Ricceri, Fulvio, Agudo, Antonio, Redondo-Sanchez, Daniel, Colorado-Yohar, Sandra M., Mokoroa, Olatz, Melander, Ole, Stocks, Tanja, Häggström, Christel, Harlid, Sophia, Bueno-de-Mesquita, Bas, van Gils, Carla H., Vermeulen, Roel Ch, Khaw, Kay-Tee, Wareham, Nicholas J., Tong, Tammy Y. N., Freisling, Heinz, Johansson, Mattias, Lennon, Hannah, AUne, Dagfinn, Ribolil, Elio, Trichopoulos, Dimitrios, Trichopoulou, Antonia, and Tsilidis, Konstantinos K.

Abstract

Several studies have reported associations of hypertension with cancer, but not all results were conclusive. We examined the association of systolic (SBP) and diastolic (DBP) blood pressure with the development of incident cancer at all anatomical sites in the European Prospective Investigation into Cancer and Nutrition (EPIC). Hazard ratios (HRs) (95% confidence intervals) were estimated using multivariable Cox proportional hazards models, stratified by EPIC-participating center and age at recruitment, and adjusted for sex, education, smoking, body mass index, physical activity, diabetes and dietary (in women also reproductive) factors. The study included 307,318 men and women, with an average follow-up of 13.7 (standard deviation 4.4) years and 39,298 incident cancers. We confirmed the expected positive association with renal cell carcinoma: HR = 1.12 (1.08-1.17) per 10 mm Hg higher SBP and HR = 1.23 (1.14-1.32) for DBP. We additionally found positive associations for esophageal squamous cell carcinoma (SCC): HR = 1.16 (1.07-1.26) (SBP), HR = 1.31 (1.13-1.51) (DBP), weaker for head and neck cancers: HR = 1.08 (1.04-1.12) (SBP), HR = 1.09 (1.01-1.17) (DBP) and, similarly, for skin SCC, colon cancer, postmenopausal breast cancer and uterine adenocarcinoma (AC), but not for esophageal AC, lung SCC, lung AC or uterine endometroid cancer. We observed weak inverse associations of SBP with cervical SCC: HR = 0.91 (0.82-1.00) and lymphomas: HR = 0.97 (0.93-1.00). There were no consistent associations with cancers in other locations. Our results are largely compatible with published studies and support weak associations of blood pressure with cancers in specific locations and morphologies.

Published
2020
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16. 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, van de Langenberg, Daniella, Vlaanderen, Jelle J, Dollé, Martijn Et, Rookus, Matti A, van Kerkhof, Linda Wm, and Vermeulen, Roel Ch

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 schedu

Published
2019

18. Searching for early breast cancer biomarkers by serum protein profiling of pre-diagnostic serum; a nested case-control study

Author

Peeters Petra HM, Grobbee Diederick E, Jönsson Bo AG, Jeppsson Marina C, Lindh Christian H, Gast Marie-Christine W, Kåredal Monica H, Krop Esmeralda JM, Opstal-van Winden Annemieke WJ, Beijnen Jos H, van Gils Carla H, and Vermeulen Roel CH

Subjects
Biomarkers, Breast cancer, Early diagnosis, 2D-nanoLC-MS/MS, Prospective, Proteomics, SELDI-TOF MS, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Serum protein profiles have been investigated frequently to discover early biomarkers for breast cancer. So far, these studies used biological samples collected at or after diagnosis. This may limit these studies' value in the search for cancer biomarkers because of the often advanced tumor stage, and consequently risk of reverse causality. We present for the first time pre-diagnostic serum protein profiles in relation to breast cancer, using the Prospect-EPIC (European Prospective Investigation into Cancer and nutrition) cohort. Methods In a nested case-control design we compared 68 women diagnosed with breast cancer within three years after enrollment, with 68 matched controls for differences in serum protein profiles. All samples were analyzed with SELDI-TOF MS (surface enhanced laser desorption/ionization time-of-flight mass spectrometry). In a subset of 20 case-control pairs, the serum proteome was identified and relatively quantified using isobaric Tags for Relative and Absolute Quantification (iTRAQ) and online two-dimensional nano-liquid chromatography coupled with tandem MS (2D-nanoLC-MS/MS). Results Two SELDI-TOF MS peaks with m/z 3323 and 8939, which probably represent doubly charged apolipoprotein C-I and C3a des-arginine anaphylatoxin (C3adesArg), were higher in pre-diagnostic breast cancer serum (p = 0.02 and p = 0.06, respectively). With 2D-nanoLC-MS/MS, afamin, apolipoprotein E and isoform 1 of inter-alpha trypsin inhibitor heavy chain H4 (ITIH4) were found to be higher in pre-diagnostic breast cancer (p < 0.05), while alpha-2-macroglobulin and ceruloplasmin were lower (p < 0.05). C3adesArg and ITIH4 have previously been related to the presence of symptomatic and/or mammographically detectable breast cancer. Conclusions We show that serum protein profiles are already altered up to three years before breast cancer detection.

Published
2011
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19. 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

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

Author

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, 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, 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, and Straif, Kurt

Published
2015

22. 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

24. Searching for early breast cancer biomarkers by serum protein profiling of pre-diagnostic serum; a nested case-control study

Author

Opstal-van Winden, Annemieke WJ, primary, Krop, Esmeralda JM, additional, Kåredal, Monica H, additional, Gast, Marie-Christine W, additional, Lindh, Christian H, additional, Jeppsson, Marina C, additional, Jönsson, Bo AG, additional, Grobbee, Diederick E, additional, Peeters, Petra HM, additional, Beijnen, Jos H, additional, van Gils, Carla H, additional, and Vermeulen, Roel CH, additional

Published
2011
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25. Impact of occupational carcinogens on lung cancer risk in a general population.

Author

De Matteis, Sara, Consonni, Dario, Lubin, Jay H, Tucker, Margaret, Peters, Susan, Vermeulen, Roel CH, Kromhout, Hans, Bertazzi, Pier Alberto, Caporaso, Neil E, Pesatori, Angela C, Wacholder, Sholom, and Landi, Maria Teresa

Subjects
PUBLISHED errata, LUNG cancer risk factors, CARCINOGENS, OCCUPATIONAL diseases, MEDICAL research, EPIDEMIOLOGY, MEDICAL publishing
Published
2013
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