1,889 results on '"Severi, Gianluca"'
Search Results
52. Inflammation and gut barrier function-related genes and colorectal cancer risk in western European populations
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Mandle, Hannah B, primary, Jenab, Mazda, additional, Gunter, Marc J, additional, Tjønneland, Anne, additional, Olsen, Anja, additional, Dahm, Christina C, additional, Zhang, Jie, additional, Sugier, Pierre-Emmanuel, additional, Rothwell, Joseph, additional, Severi, Gianluca, additional, Kaaks, Rudolf, additional, Katzke, Verena A, additional, Schulze, Matthias B, additional, Masala, Giovanna, additional, Sieri, Sabina, additional, Panico, Salvatore, additional, Sacerdote, Carlotta, additional, Bonet, Catalina, additional, Sánchez, Maria-Jose, additional, Amiano, Pilar, additional, Huerta, José María, additional, Guevara, Marcela, additional, Palmqvist, Richard, additional, Löwenmark, Thyra, additional, Perez-Cornago, Aurora, additional, Weiderpass, Elisabete, additional, Heath, Alicia K, additional, Cross, Amanda J, additional, Vineis, Paolo, additional, Hughes, David J, additional, and Fedirko, Veronika, additional
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- 2024
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53. Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study
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Laine, Jessica E, Huybrechts, Inge, Gunter, Marc J, Ferrari, Pietro, Weiderpass, Elisabete, Tsilidis, Kostas, Aune, Dagfinn, Schulze, Matthias B, Bergmann, Manuela, Temme, Elisabeth H M, Boer, Jolanda M A, Agnoli, Claudia, Ericson, Ulrika, Stubbendorff, Anna, Ibsen, Daniel B, Dahm, Christina Catherine, Deschasaux, Mélanie, Touvier, Mathilde, Kesse-Guyot, Emmanuelle, Sánchez Pérez, Maria-Jose, Rodríguez Barranco, Miguel, Tong, Tammy Y N, Papier, Keren, Knuppel, Anika, Boutron-Ruault, Marie-Christine, Mancini, Francesca, Severi, Gianluca, Srour, Bernard, Kühn, Tilman, Masala, Giovanna, Agudo, Antonio, Skeie, Guri, Rylander, Charlotta, Sandanger, Torkjel M, Riboli, Elio, and Vineis, Paolo
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- 2021
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54. Psychological burden associated with incident persistent symptoms and their evolution during the COVID-19 pandemic: a prospective population-based study
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Pignon, Baptiste, primary, Matta, Joane, additional, Wiernik, Emmanuel, additional, Toussaint, Anne, additional, Loewe, Bernd, additional, Robineau, Olivier, additional, Carrat, Fabrice, additional, Severi, Gianluca, additional, Touvier, Mathilde, additional, Gouraud, Clement, additional, Ouazana Vedrines, Charles, additional, Pitron, Victor, additional, Ranque, Brigitte, additional, Hoertel, Nicolas, additional, Kab, Sofiane, additional, Goldberg, Marcel, additional, Zins, Marie, additional, and Lemogne, Cédric, additional
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- 2024
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55. Multi-Pollutant Exposure Profiles Associated with Breast Cancer Risk: A Bayesian Profile Regression Analysis in the French E3n Cohort
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Giampiccolo, Camille, primary, Amadou, Amina, additional, Coudon, Thomas, additional, Praud, Delphine, additional, Grassot, Lény, additional, Faure, Elodie, additional, Couvidat, Florian, additional, Severi, Gianluca, additional, Mancini, Francesca Romana, additional, Fervers, Beatrice, additional, and Roy, Pascal, additional
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- 2024
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56. Inflammation-Related Marker Profiling of Dietary Patterns and All-cause Mortality in the Melbourne Collaborative Cohort Study
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Li, Sherly X, Hodge, Allison M, MacInnis, Robert J, Bassett, Julie K, Ueland, Per M, Midttun, Øivind, Ulvik, Arve, Rinaldi, Sabina, Meyer, Klaus, Navionis, Anne-Sophie, Shivappa, Nitin, Hébert, James R, Flicker, Leon, Severi, Gianluca, Jayasekara, Harindra, English, Dallas R, Vineis, Paolo, Southey, Melissa C, Milne, Roger L, Giles, Graham G, and Dugué, Pierre-Antoine
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- 2021
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57. Citrus intake and risk of skin cancer in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC)
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Mahamat-Saleh, Yahya, Cervenka, Iris, Al-Rahmoun, Marie, Mancini, Francesca R., Severi, Gianluca, Ghiasvand, Reza, Veierod, Marit B., Caini, Saverio, Palli, Domenico, Botteri, Edoardo, Sacerdote, Carlotta, Ricceri, Fulvio, Trichopoulou, Antonia, Peppa, Eleni, La Vecchia, Carlo, Overvad, Kim, Dahm, Christina C., Olsen, Anja, Tjønneland, Anne, Perez-Cornago, Aurora, Jakszyn, Paula, Grioni, Sara, Schulze, Matthias B., Skeie, Guri, Lasheras, Cristina, Colorado-Yohar, Sandra, Rodríguez-Barranco, Miguel, Kühn, Tilman, Katzke, Verena A., Amiano, Pilar, Tumino, Rosario, Panico, Salvatore, Ezponda, Ana, Sonestedt, Emily, Scalbert, Augustin, Weiderpass, Elisabete, Boutron-Ruault, Marie-Christine, and Kvaskoff, Marina
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- 2020
58. Prospective analysis of circulating metabolites and endometrial cancer risk
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Dossus, Laure, Kouloura, Eirini, Biessy, Carine, Viallon, Vivian, Siskos, Alexandros P., Dimou, Niki, Rinaldi, Sabina, Merritt, Melissa A., Allen, Naomi, Fortner, Renee, Kaaks, Rudolf, Weiderpass, Elisabete, Gram, Inger T., Rothwell, Joseph A., Lécuyer, Lucie, Severi, Gianluca, Schulze, Matthias B., Nøst, Therese Haugdahl, Crous-Bou, Marta, Sánchez, Maria-Jose, Amiano, Pilar, Colorado-Yohar, Sandra M., Gurrea, Aurelio Barricarte, Schmidt, Julie A., Palli, Domenico, Agnoli, Claudia, Tumino, Rosario, Sacerdote, Carlotta, Mattiello, Amalia, Vermeulen, Roel, Heath, Alicia K., Christakoudi, Sofia, Tsilidis, Konstantinos K., Travis, Ruth C., Gunter, Marc J., and Keun, Hector C.
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- 2021
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59. Body size and dietary risk factors for aggressive prostate cancer : a case–control study
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Pal, Mikaela, Hodge, Allison M., Papa, Nathan, MacInnis, Robert J., Bassett, Julie K., Bolton, Damien, Davis, Ian D., Millar, Jeremy, English, Dallas R., Hopper, John L., Severi, Gianluca, Southey, Melissa C., Milne, Roger L., and Giles, Graham G.
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- 2019
60. Monitoring the proportion of the population infected by SARS-CoV-2 using age-stratified hospitalisation and serological data: a modelling study
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Hozé, Nathanaël, Paireau, Juliette, Lapidus, Nathanaël, Tran Kiem, Cécile, Salje, Henrik, Severi, Gianluca, Touvier, Mathilde, Zins, Marie, de Lamballerie, Xavier, Lévy-Bruhl, Daniel, Carrat, Fabrice, and Cauchemez, Simon
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- 2021
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61. Household Cleaning and Poor Asthma Control Among Elderly Women
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Dumas, Orianne, Bédard, Annabelle, Marbac, Matthieu, Sedki, Mohammed, Temam, Sofia, Chanoine, Sébastien, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Garcia-Aymerich, Judith, Siroux, Valérie, Varraso, Raphaëlle, and Le Moual, Nicole
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- 2021
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62. Long-term atmospheric exposure to PCB153 and breast cancer risk in a case-control study nested in the French E3N cohort from 1990 to 2011
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Deygas, Floriane, Amadou, Amina, Coudon, Thomas, Grassot, Lény, Couvidat, Florian, Bessagnet, Bertrand, Faure, Elodie, Salizzoni, Pietro, Gulliver, John, Caudeville, Julien, Severi, Gianluca, Mancini, Francesca Romana, Leffondré, Karen, Fervers, Béatrice, and Praud, Delphine
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- 2021
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63. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study
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Haycock, Philip C, Burgess, Stephen, Nounu, Aayah, Zheng, Jie, Okoli, George N, Bowden, Jack, Wade, Kaitlin Hazel, Timpson, Nicholas J, Evans, David M, Willeit, Peter, Aviv, Abraham, Gaunt, Tom R, Hemani, Gibran, Mangino, Massimo, Ellis, Hayley Patricia, Kurian, Kathreena M, Pooley, Karen A, Eeles, Rosalind A, Lee, Jeffrey E, Fang, Shenying, Chen, Wei V, Law, Matthew H, Bowdler, Lisa M, Iles, Mark M, Yang, Qiong, Worrall, Bradford B, Markus, Hugh Stephen, Hung, Rayjean J, Amos, Chris I, Spurdle, Amanda B, Thompson, Deborah J, O’Mara, Tracy A, Wolpin, Brian, Amundadottir, Laufey, Stolzenberg-Solomon, Rachael, Trichopoulou, Antonia, Onland-Moret, N Charlotte, Lund, Eiliv, Duell, Eric J, Canzian, Federico, Severi, Gianluca, Overvad, Kim, Gunter, Marc J, Tumino, Rosario, Svenson, Ulrika, van Rij, Andre, Baas, Annette F, Bown, Matthew J, Samani, Nilesh J, van t’Hof, Femke NG, Tromp, Gerard, Jones, Gregory T, Kuivaniemi, Helena, Elmore, James R, Johansson, Mattias, Mckay, James, Scelo, Ghislaine, Carreras-Torres, Robert, Gaborieau, Valerie, Brennan, Paul, Bracci, Paige M, Neale, Rachel E, Olson, Sara H, Gallinger, Steven, Li, Donghui, Petersen, Gloria M, Risch, Harvey A, Klein, Alison P, Han, Jiali, Abnet, Christian C, Freedman, Neal D, Taylor, Philip R, Maris, John M, Aben, Katja K, Kiemeney, Lambertus A, Vermeulen, Sita H, Wiencke, John K, Walsh, Kyle M, Wrensch, Margaret, Rice, Terri, Turnbull, Clare, Litchfield, Kevin, Paternoster, Lavinia, Standl, Marie, Abecasis, Gonçalo R, SanGiovanni, John Paul, Li, Yong, Mijatovic, Vladan, Sapkota, Yadav, Low, Siew-Kee, Zondervan, Krina T, Montgomery, Grant W, Nyholt, Dale R, van Heel, David A, Hunt, Karen, Arking, Dan E, Ashar, Foram N, Sotoodehnia, Nona, Woo, Daniel, and Rosand, Jonathan
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Rare Diseases ,Clinical Research ,Cancer ,Prevention ,Genetics ,Aetiology ,2.1 Biological and endogenous factors ,Adult ,Aged ,Aged ,80 and over ,Cardiovascular Diseases ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Germ-Line Mutation ,Humans ,Male ,Mendelian Randomization Analysis ,Middle Aged ,Neoplasms ,Polymorphism ,Single Nucleotide ,Risk Assessment ,Telomere ,Telomere Homeostasis ,Telomeres Mendelian Randomization Collaboration ,Public Health and Health Services ,Oncology and carcinogenesis - Abstract
ImportanceThe causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation.ObjectiveTo conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases.Data sourcesGenomewide association studies (GWAS) published up to January 15, 2015.Study selectionGWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available.Data extraction and synthesisSummary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population.Main outcomes and measuresOdds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation.ResultsSummary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95% CI, 0.05-0.15]).Conclusions and relevanceIt is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases.
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- 2017
64. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study.
- Author
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Telomeres Mendelian Randomization Collaboration, Haycock, Philip C, Burgess, Stephen, Nounu, Aayah, Zheng, Jie, Okoli, George N, Bowden, Jack, Wade, Kaitlin Hazel, Timpson, Nicholas J, Evans, David M, Willeit, Peter, Aviv, Abraham, Gaunt, Tom R, Hemani, Gibran, Mangino, Massimo, Ellis, Hayley Patricia, Kurian, Kathreena M, Pooley, Karen A, Eeles, Rosalind A, Lee, Jeffrey E, Fang, Shenying, Chen, Wei V, Law, Matthew H, Bowdler, Lisa M, Iles, Mark M, Yang, Qiong, Worrall, Bradford B, Markus, Hugh Stephen, Hung, Rayjean J, Amos, Chris I, Spurdle, Amanda B, Thompson, Deborah J, O'Mara, Tracy A, Wolpin, Brian, Amundadottir, Laufey, Stolzenberg-Solomon, Rachael, Trichopoulou, Antonia, Onland-Moret, N Charlotte, Lund, Eiliv, Duell, Eric J, Canzian, Federico, Severi, Gianluca, Overvad, Kim, Gunter, Marc J, Tumino, Rosario, Svenson, Ulrika, van Rij, Andre, Baas, Annette F, Bown, Matthew J, Samani, Nilesh J, van t'Hof, Femke NG, Tromp, Gerard, Jones, Gregory T, Kuivaniemi, Helena, Elmore, James R, Johansson, Mattias, Mckay, James, Scelo, Ghislaine, Carreras-Torres, Robert, Gaborieau, Valerie, Brennan, Paul, Bracci, Paige M, Neale, Rachel E, Olson, Sara H, Gallinger, Steven, Li, Donghui, Petersen, Gloria M, Risch, Harvey A, Klein, Alison P, Han, Jiali, Abnet, Christian C, Freedman, Neal D, Taylor, Philip R, Maris, John M, Aben, Katja K, Kiemeney, Lambertus A, Vermeulen, Sita H, Wiencke, John K, Walsh, Kyle M, Wrensch, Margaret, Rice, Terri, Turnbull, Clare, Litchfield, Kevin, Paternoster, Lavinia, Standl, Marie, Abecasis, Gonçalo R, SanGiovanni, John Paul, Li, Yong, Mijatovic, Vladan, Sapkota, Yadav, Low, Siew-Kee, Zondervan, Krina T, Montgomery, Grant W, Nyholt, Dale R, van Heel, David A, Hunt, Karen, Arking, Dan E, Ashar, Foram N, Sotoodehnia, Nona, and Woo, Daniel
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Telomeres Mendelian Randomization Collaboration ,Telomere ,Humans ,Neoplasms ,Cardiovascular Diseases ,Genetic Predisposition to Disease ,Risk Assessment ,Germ-Line Mutation ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Aged ,80 and over ,Middle Aged ,Female ,Male ,Genome-Wide Association Study ,Mendelian Randomization Analysis ,Telomere Homeostasis ,Polymorphism ,Single Nucleotide ,and over ,Prevention ,Clinical Research ,Cancer ,Genetics ,Rare Diseases ,2.1 Biological and endogenous factors ,Oncology and Carcinogenesis ,Public Health and Health Services - Abstract
ImportanceThe causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation.ObjectiveTo conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases.Data sourcesGenomewide association studies (GWAS) published up to January 15, 2015.Study selectionGWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available.Data extraction and synthesisSummary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population.Main outcomes and measuresOdds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation.ResultsSummary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95% CI, 0.05-0.15]).Conclusions and relevanceIt is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases.
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- 2017
65. Investigation of circulating metabolites associated with breast cancer risk by untargeted metabolomics: a case–control study nested within the French E3N cohort
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Jobard, Elodie, Dossus, Laure, Baglietto, Laura, Fornili, Marco, Lécuyer, Lucie, Mancini, Francesca Romana, Gunter, Marc J., Trédan, Olivier, Boutron-Ruault, Marie-Christine, Elena-Herrmann, Bénédicte, Severi, Gianluca, and Rothwell, Joseph A.
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- 2021
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66. Domestic exposure to irritant cleaning agents and asthma in women
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Lemire, Pierre, Dumas, Orianne, Chanoine, Sébastien, Temam, Sofia, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Zock, Jan-Paul, Siroux, Valérie, Varraso, Raphaëlle, and Le Moual, Nicole
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- 2020
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67. Pre‐diagnostic circulating resistin concentrations and mortality among individuals with colorectal cancer: Results from the European Prospective Investigation into Cancer and Nutrition study.
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Pham, Thu Thi, Nimptsch, Katharina, Aleksandrova, Krasimira, Jenab, Mazda, Fedirko, Veronika, Wu, Kana, Eriksen, Anne Kirstine, Tjønneland, Anne, Severi, Gianluca, Rothwell, Joseph, Kaaks, Rudolf, Katzke, Verena, Catalano, Alberto, Agnoli, Claudia, Masala, Giovanna, De Magistris, Maria Santucci, Tumino, Rosario, Vermeulen, Roel, Aizpurua, Amaia, and Trobajo‐Sanmartín, Camino
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RESISTIN ,COLORECTAL cancer ,PROPORTIONAL hazards models ,BODY mass index - Abstract
Resistin is a protein involved in inflammation and angiogenesis processes and may play a role in the progression of colorectal cancer (CRC). However, it remains unclear whether resistin is associated with increased mortality after CRC diagnosis. We examined pre‐diagnostic serum resistin concentrations in relation to CRC‐specific and all‐cause mortality among 1343 incident CRC cases from the European Prospective Investigation into Cancer and Nutrition cohort. For CRC‐specific mortality as the primary outcome, hazard ratios (HRs) and 95% confidence intervals (95% CI) were estimated from competing risk analyses based on cause‐specific Cox proportional hazards models and further in sensitivity analyses using Fine–Gray proportional subdistribution hazards models. For all‐cause mortality as the secondary outcome, Cox proportional hazards models were used. Subgroup analyses were performed by sex, tumor subsite, tumor stage, body mass index and time to CRC diagnosis. Resistin was measured on a median of 4.8 years before CRC diagnosis. During a median follow‐up of 8.2 years, 474 deaths from CRC and 147 deaths from other causes were observed. Resistin concentrations were not associated with CRC‐specific mortality (HRQ4vsQ1 = 0.95, 95% CI: 0.73–1.23; Ptrend =.97; and HRper doubling of resistin concentration = 1.00; 95% CI: 0.84–1.19; P =.98) or all‐cause mortality. Results from competing risk (sensitivity) analysis were similar. No associations were found in any subgroup analyses. These findings suggest no association between pre‐diagnostic circulating resistin concentrations and CRC‐specific or all‐cause mortality among persons with CRC, and the potential insignificance of resistin in CRC progression. [ABSTRACT FROM AUTHOR]
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- 2024
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68. Consumption of Fish and Long-chain n-3 Polyunsaturated Fatty Acids Is Associated With Reduced Risk of Colorectal Cancer in a Large European Cohort
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Aglago, Elom K., Huybrechts, Inge, Murphy, Neil, Casagrande, Corinne, Nicolas, Genevieve, Pischon, Tobias, Fedirko, Veronika, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Fournier, Agnès, Katzke, Verena, Kühn, Tilman, Olsen, Anja, Tjønneland, Anne, Dahm, Christina C., Overvad, Kim, Lasheras, Cristina, Agudo, Antonio, Sánchez, Maria-Jose, Amiano, Pilar, Huerta, José Maria, Ardanaz, Eva, Perez-Cornago, Aurora, Trichopoulou, Antonia, Karakatsani, Anna, Martimianaki, Georgia, Palli, Domenico, Pala, Valeria, Tumino, Rosario, Naccarati, Alessio, Panico, Salvatore, Bueno-de-Mesquita, Bas, May, Anne, Derksen, Jeroen W.G., Hellstrand, Sophie, Ohlsson, Bodil, Wennberg, Maria, Van Guelpen, Bethany, Skeie, Guri, Brustad, Magritt, Weiderpass, Elisabete, Cross, Amanda J., Ward, Heather, Riboli, Elio, Norat, Teresa, Chajes, Veronique, and Gunter, Marc J.
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- 2020
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69. The causal relevance of body mass index in different histological types of lung cancer: A Mendelian randomization study.
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Carreras-Torres, Robert, Haycock, Philip C, Relton, Caroline L, Martin, Richard M, Smith, George Davey, Kraft, Peter, Gao, Chi, Tworoger, Shelley, Le Marchand, Loïc, Wilkens, Lynne R, Park, Sungshim L, Haiman, Christopher, Field, John K, Davies, Michael, Marcus, Michael, Liu, Geoffrey, Caporaso, Neil E, Christiani, David C, Wei, Yongyue, Chen, Chu, Doherty, Jennifer A, Severi, Gianluca, Goodman, Gary E, Hung, Rayjean J, Amos, Christopher I, McKay, James, Johansson, Mattias, and Brennan, Paul
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Humans ,Lung Neoplasms ,Body Mass Index ,Risk Factors ,Case-Control Studies ,Smoking ,Female ,Male ,Mendelian Randomization Analysis - Abstract
Body mass index (BMI) is inversely associated with lung cancer risk in observational studies, even though it increases the risk of several other cancers, which could indicate confounding by tobacco smoking or reverse causality. We used the two-sample Mendelian randomization (MR) approach to circumvent these limitations of observational epidemiology by constructing a genetic instrument for BMI, based on results from the GIANT consortium, which was evaluated in relation to lung cancer risk using GWAS results on 16,572 lung cancer cases and 21,480 controls. Results were stratified by histological subtype, smoking status and sex. An increase of one standard deviation (SD) in BMI (4.65 Kg/m(2)) raised the risk for lung cancer overall (OR = 1.13; P = 0.10). This was driven by associations with squamous cell (SQ) carcinoma (OR = 1.45; P = 1.2 × 10(-3)) and small cell (SC) carcinoma (OR = 1.81; P = 0.01). An inverse trend was seen for adenocarcinoma (AD) (OR = 0.82; P = 0.06). In stratified analyses, a 1 SD increase in BMI was inversely associated with overall lung cancer in never smokers (OR = 0.50; P = 0.02). These results indicate that higher BMI may increase the risk of certain types of lung cancer, in particular SQ and SC carcinoma.
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- 2016
70. A Meta-analysis of Individual Participant Data Reveals an Association between Circulating Levels of IGF-I and Prostate Cancer Risk
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Travis, Ruth C, Appleby, Paul N, Martin, Richard M, Holly, Jeff MP, Albanes, Demetrius, Black, Amanda, Bueno-de-Mesquita, HB As, Chan, June M, Chen, Chu, Chirlaque, Maria-Dolores, Cook, Michael B, Deschasaux, Mélanie, Donovan, Jenny L, Ferrucci, Luigi, Galan, Pilar, Giles, Graham G, Giovannucci, Edward L, Gunter, Marc J, Habel, Laurel A, Hamdy, Freddie C, Helzlsouer, Kathy J, Hercberg, Serge, Hoover, Robert N, Janssen, Joseph AMJL, Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Metter, E Jeffrey, Mikami, Kazuya, Morris, Joan K, Neal, David E, Neuhouser, Marian L, Ozasa, Kotaro, Palli, Domenico, Platz, Elizabeth A, Pollak, Michael, Price, Alison J, Roobol, Monique J, Schaefer, Catherine, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Stattin, Pär, Tamakoshi, Akiko, Tangen, Catherine M, Touvier, Mathilde, Wald, Nicholas J, Weiss, Noel S, Ziegler, Regina G, Key, Timothy J, and Allen, Naomi E
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Aging ,Prostate Cancer ,Cancer ,Urologic Diseases ,Aged ,Humans ,Insulin-Like Growth Factor I ,Male ,Middle Aged ,Prostatic Neoplasms ,Risk Factors ,Oncology & Carcinogenesis ,Biochemistry and cell biology ,Oncology and carcinogenesis - Abstract
The role of insulin-like growth factors (IGF) in prostate cancer development is not fully understood. To investigate the association between circulating concentrations of IGFs (IGF-I, IGF-II, IGFBP-1, IGFBP-2, and IGFBP-3) and prostate cancer risk, we pooled individual participant data from 17 prospective and two cross-sectional studies, including up to 10,554 prostate cancer cases and 13,618 control participants. Conditional logistic regression was used to estimate the ORs for prostate cancer based on the study-specific fifth of each analyte. Overall, IGF-I, IGF-II, IGFBP-2, and IGFBP-3 concentrations were positively associated with prostate cancer risk (Ptrend all ≤ 0.005), and IGFBP-1 was inversely associated weakly with risk (Ptrend = 0.05). However, heterogeneity between the prospective and cross-sectional studies was evident (Pheterogeneity = 0.03), unless the analyses were restricted to prospective studies (with the exception of IGF-II, Pheterogeneity = 0.02). For prospective studies, the OR for men in the highest versus the lowest fifth of each analyte was 1.29 (95% confidence interval, 1.16-1.43) for IGF-I, 0.81 (0.68-0.96) for IGFBP-1, and 1.25 (1.12-1.40) for IGFBP-3. These associations did not differ significantly by time-to-diagnosis or tumor stage or grade. After mutual adjustment for each of the other analytes, only IGF-I remained associated with risk. Our collaborative study represents the largest pooled analysis of the relationship between prostate cancer risk and circulating concentrations of IGF-I, providing strong evidence that IGF-I is highly likely to be involved in prostate cancer development. Cancer Res; 76(8); 2288-300. ©2016 AACR.
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- 2016
71. Fine mapping of chromosome 5p15.33 based on a targeted deep sequencing and high density genotyping identifies novel lung cancer susceptibility loci
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Kachuri, Linda, Amos, Christopher I, McKay, James D, Johansson, Mattias, Vineis, Paolo, Bueno-de-Mesquita, H Bas, Boutron-Ruault, Marie-Christine, Johansson, Mikael, Quirós, J Ramón, Sieri, Sabina, Travis, Ruth C, Weiderpass, Elisabete, Le Marchand, Loic, Henderson, Brian E, Wilkens, Lynne, Goodman, Gary E, Chen, Chu, Doherty, Jennifer A, Christiani, David C, Wei, Yongyue, Su, Li, Tworoger, Shelley, Zhang, Xuehong, Kraft, Peter, Zaridze, David, Field, John K, Marcus, Michael W, Davies, Michael PA, Hyde, Russell, Caporaso, Neil E, Landi, Maria Teresa, Severi, Gianluca, Giles, Graham G, Liu, Geoffrey, McLaughlin, John R, Li, Yafang, Xiao, Xiangjun, Fehringer, Gord, Zong, Xuchen, Denroche, Robert E, Zuzarte, Philip C, McPherson, John D, Brennan, Paul, and Hung, Rayjean J
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Lung ,Human Genome ,Genetics ,Cancer ,Prevention ,Lung Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Case-Control Studies ,Chromosome Mapping ,Chromosomes ,Human ,Pair 5 ,Female ,Genetic Loci ,Genetic Predisposition to Disease ,Genotyping Techniques ,Humans ,Lung Neoplasms ,Male ,Middle Aged ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
Chromosome 5p15.33 has been identified as a lung cancer susceptibility locus, however the underlying causal mechanisms were not fully elucidated. Previous fine-mapping studies of this locus have relied on imputation or investigated a small number of known, common variants. This study represents a significant advance over previous research by investigating a large number of novel, rare variants, as well as their underlying mechanisms through telomere length. Variants for this fine-mapping study were identified through a targeted deep sequencing (average depth of coverage greater than 4000×) of 576 individuals. Subsequently, 4652 SNPs, including 1108 novel SNPs, were genotyped in 5164 cases and 5716 controls of European ancestry. After adjusting for known risk loci, rs2736100 and rs401681, we identified a new, independent lung cancer susceptibility variant in LPCAT1: rs139852726 (OR = 0.46, P = 4.73×10(-9)), and three new adenocarcinoma risk variants in TERT: rs61748181 (OR = 0.53, P = 2.64×10(-6)), rs112290073 (OR = 1.85, P = 1.27×10(-5)), rs138895564 (OR = 2.16, P = 2.06×10(-5); among young cases, OR = 3.77, P = 8.41×10(-4)). In addition, we found that rs139852726 (P = 1.44×10(-3)) was associated with telomere length in a sample of 922 healthy individuals. The gene-based SKAT-O analysis implicated TERT as the most relevant gene in the 5p15.33 region for adenocarcinoma (P = 7.84×10(-7)) and lung cancer (P = 2.37×10(-5)) risk. In this largest fine-mapping study to investigate a large number of rare and novel variants within 5p15.33, we identified novel lung and adenocarcinoma susceptibility loci with large effects and provided support for the role of telomere length as the potential underlying mechanism.
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- 2016
72. Childhood and adulthood passive and active smoking, and the ABO group as risk factors for pancreatic cancer in women
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Vedie, Anne‐Laure, primary, Laouali, Nasser, additional, Gelot, Amandine, additional, Severi, Gianluca, additional, Boutron‐Ruault, Marie‐Christine, additional, and Rebours, Vinciane, additional
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- 2023
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73. Long-term exposure to ambient air pollution and risk of leukemia and lymphoma in a pooled European cohort
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Taj, Tahir, primary, Chen, Jie, additional, Rodopoulou, Sophia, additional, Strak, Maciej, additional, de Hoogh, Kees, additional, Poulsen, Aslak Harbo, additional, Andersen, Zorana J., additional, Bellander, Tom, additional, Brandt, Jørgen, additional, Zitt, Emanuel, additional, Fecht, Daniela, additional, Forastiere, Francesco, additional, Gulliver, John, additional, Hertel, Ole, additional, Hoffmann, Barbara, additional, Hvidtfeldt, Ulla Arthur, additional, Jørgensen, Jeanette T., additional, Katsouyanni, Klea, additional, Ketzel, Matthias, additional, Lager, Anton, additional, Leander, Karin, additional, Liu, Shuo, additional, Ljungman, Petter, additional, Severi, Gianluca, additional, Besson, Caroline, additional, Magnusson, Patrik K.E., additional, Nagel, Gabriele, additional, Pershagen, Göran, additional, Peters, Annette, additional, Rizzuto, Debora, additional, Samoli, Evangelia, additional, Sørensen, Mette, additional, Stafoggia, Massimo, additional, Tjønneland, Anne, additional, Weinmayr, Gudrun, additional, Wolf, Kathrin, additional, Brunekreef, Bert, additional, Hoek, Gerard, additional, and Raaschou-Nielsen, Ole, additional
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- 2023
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74. Depressive symptoms and gender differences in the risk of post-COVID-19 persistent symptoms: a prospective population-based cohort study
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Lemogne, Cédric, primary, Matta, Joane, additional, Pignon, Baptiste, additional, Robineau, Olivier, additional, Carrat, Fabrice, additional, Severi, Gianluca, additional, Touvier, Mathilde, additional, Blanché, Hélène, additional, Deleuze, Jean-François, additional, Gouraud, Clément, additional, Vedrines, Charles Ouazana, additional, Pitron, Victor, additional, Tebeka, Sarah, additional, Ranque, Brigitte, additional, Hoertel, Nicolas, additional, Kab, Sofiane, additional, Goldberg, Marcel, additional, and Zins, Marie, additional
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- 2023
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75. Long-term exposure to several constituents and sources of PM2.5 is associated with incidence of upper aerodigestive tract cancers but not gastric cancer: Results from the large pooled European cohort of the ELAPSE project
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Weinmayr, Gudrun, primary, Chen, Jie, additional, Jaensch, Andrea, additional, Skodda, Lea, additional, Rodopoulou, Sophia, additional, Strak, Maciej, additional, de Hoogh, Kees, additional, Andersen, Zorana J., additional, Bellander, Tom, additional, Brandt, Jørgen, additional, Fecht, Daniela, additional, Forastiere, Francesco, additional, Gulliver, John, additional, Hertel, Ole, additional, Hoffmann, Barbara, additional, Hvidtfeldt, Ulla Arthur, additional, Katsouyanni, Klea, additional, Ketzel, Matthias, additional, Leander, Karin, additional, Magnusson, Patrik K.E., additional, Pershagen, Göran, additional, Rizzuto, Debora, additional, Samoli, Evangelia, additional, Severi, Gianluca, additional, Stafoggia, Massimo, additional, Tjønneland, Anne, additional, Vermeulen, Roel, additional, Wolf, Kathrin, additional, Zitt, Emanuel, additional, Brunekreef, Bert, additional, Thurston, George, additional, Hoek, Gerard, additional, Raaschou-Nielsen, Ole, additional, and Nagel, Gabriele, additional
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- 2023
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76. Stem cell replication, somatic mutations and role of randomness in the development of cancer
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Perduca, Vittorio, Alexandrov, Ludmil B., Kelly-Irving, Michelle, Delpierre, Cyrille, Omichessan, Hanane, Little, Mark P., Vineis, Paolo, and Severi, Gianluca
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- 2019
77. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies 1–3
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Key, Timothy J, Appleby, Paul N, Travis, Ruth C, Albanes, Demetrius, Alberg, Anthony J, Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H Bas, Chan, June M, Chen, Chu, Cook, Michael B, Donovan, Jenny L, Galan, Pilar, Gilbert, Rebecca, Giles, Graham G, Giovannucci, Edward, Goodman, Gary E, Goodman, Phyllis J, Gunter, Marc J, Hamdy, Freddie C, Heliövaara, Markku, Helzlsouer, Kathy J, Henderson, Brian E, Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N, Johansson, Mattias, Khaw, Kay-Tee, King, Irena B, Knekt, Paul, Kolonel, Laurence N, Le Marchand, Loic, Männistö, Satu, Martin, Richard M, Meyer, Haakon E, Mondul, Alison M, Moy, Kristin A, Neal, David E, Neuhouser, Marian L, Palli, Domenico, Platz, Elizabeth A, Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Tjønneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J, Ziegler, Regina G, Zhou, Cindy Ke, Allen, Naomi E, Biomarkers, Endogenous Hormones Nutritional, and Group, Prostate Cancer Collaborative
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Prevention ,Urologic Diseases ,Nutrition ,Prostate Cancer ,Cancer ,Aging ,Clinical Research ,Adult ,Biomarkers ,Carotenoids ,Case-Control Studies ,Cohort Studies ,Cross-Sectional Studies ,Humans ,Lycopene ,Male ,Meta-Analysis as Topic ,Middle Aged ,Neoplasm Grading ,Neoplasm Staging ,Observational Studies as Topic ,Prospective Studies ,Prostate ,Prostatic Neoplasms ,Risk Factors ,Vitamin A ,alpha-Tocopherol ,prostate cancer ,carotenoids ,retinol ,tocopherols ,vitamin E ,vitamin A ,pooled analysis ,nested case-control study ,biomarkers ,Endogenous Hormones Nutritional Biomarkers Prostate Cancer Collaborative Group ,Engineering ,Medical and Health Sciences ,Nutrition & Dietetics ,Clinical sciences ,Nutrition and dietetics - Abstract
BackgroundIndividual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease.ObjectiveThe objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors.DesignPrincipal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets.ResultsData were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For α-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). γ-Tocopherol was not associated with risk.ConclusionsOverall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.
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- 2015
78. Corrigendum: genome-wide association study of colorectal cancer identifies six new susceptibility loci.
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Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B
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MD Multidisciplinary - Published
- 2015
79. Erratum: Corrigendum: Genome-wide association study of colorectal cancer identifies six new susceptibility loci
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Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B
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Biological Sciences ,Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Digestive Diseases ,Cancer ,Colo-Rectal Cancer - Published
- 2015
80. Use of systemic glucocorticoids and risk of breast cancer in a prospective cohort of postmenopausal women
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Cairat, Manon, Al Rahmoun, Marie, Gunter, Marc J., Heudel, Pierre-Etienne, Severi, Gianluca, Dossus, Laure, and Fournier, Agnès
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- 2021
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81. Lifestyle correlates of eight breast cancer-related metabolites: a cross-sectional study within the EPIC cohort
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His, Mathilde, Viallon, Vivian, Dossus, Laure, Schmidt, Julie A., Travis, Ruth C., Gunter, Marc J., Overvad, Kim, Kyrø, Cecilie, Tjønneland, Anne, Lécuyer, Lucie, Rothwell, Joseph A., Severi, Gianluca, Johnson, Theron, Katzke, Verena, Schulze, Matthias B., Masala, Giovanna, Sieri, Sabina, Panico, Salvatore, Tumino, Rosario, Macciotta, Alessandra, Boer, Jolanda M. A., Monninkhof, Evelyn M., Olsen, Karina Standahl, Nøst, Therese H., Sandanger, Torkjel M., Agudo, Antonio, Sánchez, Maria-Jose, Amiano, Pilar, Colorado-Yohar, Sandra M., Ardanaz, Eva, Vidman, Linda, Winkvist, Anna, Heath, Alicia K., Weiderpass, Elisabete, Huybrechts, Inge, and Rinaldi, Sabina
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- 2021
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82. Exposure to airborne cadmium and breast cancer stage, grade and histology at diagnosis: findings from the E3N cohort study
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Amadou, Amina, Praud, Delphine, Coudon, Thomas, Danjou, Aurélie M. N., Faure, Elodie, Deygas, Floriane, Grassot, Lény, Leffondré, Karen, Severi, Gianluca, Salizzoni, Pietro, Mancini, Francesca Romana, and Fervers, Béatrice
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- 2021
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83. Development and validation of a lifestyle-based model for colorectal cancer risk prediction: the LiFeCRC score
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Aleksandrova, Krasimira, Reichmann, Robin, Kaaks, Rudolf, Jenab, Mazda, Bueno-de-Mesquita, H. Bas, Dahm, Christina C., Eriksen, Anne Kirstine, Tjønneland, Anne, Artaud, Fanny, Boutron-Ruault, Marie-Christine, Severi, Gianluca, Hüsing, Anika, Trichopoulou, Antonia, Karakatsani, Anna, Peppa, Eleni, Panico, Salvatore, Masala, Giovanna, Grioni, Sara, Sacerdote, Carlotta, Tumino, Rosario, Elias, Sjoerd G., May, Anne M., Borch, Kristin B., Sandanger, Torkjel M., Skeie, Guri, Sánchez, Maria-Jose, Huerta, José María, Sala, Núria, Gurrea, Aurelio Barricarte, Quirós, José Ramón, Amiano, Pilar, Berntsson, Jonna, Drake, Isabel, van Guelpen, Bethany, Harlid, Sophia, Key, Tim, Weiderpass, Elisabete, Aglago, Elom K., Cross, Amanda J., Tsilidis, Konstantinos K., Riboli, Elio, and Gunter, Marc J.
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- 2021
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84. Autoimmunity plays a role in the onset of diabetes after 40 years of age
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Rolandsson, Olov, Hampe, Christiane S., Sharp, Stephen J., Ardanaz, Eva, Boeing, Heiner, Fagherazzi, Guy, Mancini, Francesca Romana, Nilsson, Peter M., Overvad, Kim, Chirlaque, Maria-Dolores, Dorronsoro, Miren, Gunter, Marc J., Kaaks, Rudolf, Key, Timothy J., Khaw, Kay-Tee, Krogh, Vittorio, Kühn, Tilman, Palli, Domenico, Panico, Salvatore, Sacerdote, Carlotta, Sánchez, Maria-José, Severi, Gianluca, Spijkerman, Annemieke M. W., Tumino, Rosario, van der Schouw, Yvonne T., Riboli, Elio, Forouhi, Nita G., Langenberg, Claudia, and Wareham, Nicholas J.
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- 2020
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85. Genome-wide association study of colorectal cancer identifies six new susceptibility loci.
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Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stéphane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, and Zheng, Wei
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Humans ,Colorectal Neoplasms ,Genetic Predisposition to Disease ,Odds Ratio ,Case-Control Studies ,Polymorphism ,Single Nucleotide ,Genome-Wide Association Study ,Genetics ,Digestive Diseases ,Prevention ,Cancer ,Human Genome ,Colo-Rectal Cancer ,2.1 Biological and endogenous factors ,MD Multidisciplinary - Abstract
Genetic susceptibility to colorectal cancer is caused by rare pathogenic mutations and common genetic variants that contribute to familial risk. Here we report the results of a two-stage association study with 18,299 cases of colorectal cancer and 19,656 controls, with follow-up of the most statistically significant genetic loci in 4,725 cases and 9,969 controls from two Asian consortia. We describe six new susceptibility loci reaching a genome-wide threshold of P
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- 2015
86. A Prospective Study of the Immune System Activation Biomarker Neopterin and Colorectal Cancer Risk
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Aleksandrova, Krasimira, Chuang, Shu-Chun, Boeing, Heiner, Zuo, Hui, Tell, Grethe S, Pischon, Tobias, Jenab, Mazda, Bueno-de-Mesquita, Bas, Vollset, Stein Emil, Midttun, Øivind, Ueland, Per Magne, Fedirko, Veronika, Johansson, Mattias, Weiderpass, Elisabete, Severi, Gianluca, Racine, Antoine, Boutron-Ruault, Marie-Christine, Kaaks, Rudolf, Kühn, Tilman, Tjønneland, Anne, Overvad, Kim, Quirós, J Ramón, Jakszyn, Paula, Sánchez, María-José, Dorronsoro, Miren, Chirlaque, Maria-Dolores, Ardanaz, Eva, Khaw, Kay-Tee, Wareham, Nicholas J, Travis, Ruth C, Trichopoulou, Antonia, Lagiou, Pagona, Trichopoulos, Dimitrios, Palli, Domenico, Sieri, Sabina, Tumino, Rosario, Panico, Salvatore, May, Anne M, Palmqvist, Richard, Ljuslinder, Ingrid, Kong, So Yeon J, Freisling, Heinz, Gunter, Marc J, Lu, Yunxia, Cross, Amanda J, Riboli, Elio, and Vineis, Paolo
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Colo-Rectal Cancer ,Cancer ,Clinical Research ,Digestive Diseases ,Adult ,Aged ,Biomarkers ,Tumor ,Case-Control Studies ,Chromatography ,Liquid ,Colonic Neoplasms ,Colorectal Neoplasms ,Europe ,Female ,Humans ,Immunity ,Cellular ,Male ,Middle Aged ,Neopterin ,Odds Ratio ,Prospective Studies ,Rectal Neoplasms ,Sensitivity and Specificity ,T-Lymphocytes ,Helper-Inducer ,Tandem Mass Spectrometry ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
Neopterin may be relevant for colorectal cancer (CRC) development, as a biomarker of cellular immune activity exerting pleiotropic effects on cellular ageing, oxidative stress, and inflammation. So far, the association between prediagnostic neopterin and colon and rectal cancer risk has not been evaluated in human populations. A nested case-control study was conducted within the European Prospective Investigation into Cancer and Nutrition cohort using data on plasma concentrations of total neopterin (T-N, sum of neopterin and 7,8-dihydroneopterin) in 830 incident CRC case patients (561 colon and 269 rectal) matched within risk sets to 830 control participants. A subsequent replication study used data from the Hordaland Health Study, where 173 CRC case patients have been diagnosed among 6594 healthy participants over 12 years of follow-up. After multivariable adjustment for a priori chosen CRC risk factors, a "U-shaped" association of T-N with CRC was revealed. Compared with the second quintile of the T-N distribution, the relative risks for the first, third, fourth, and fifth quintiles were 2.37 (95% CI = 1.66 to 3.39), 1.24 (95% CI = 0.87 to 1.77), 1.55 (95% CI = 1.08 to 2.22), and 2.31 (95% CI = 1.63 to 3.27), respectively. Replication of these associations within the Hordaland Health Study yielded similar results. No differences have been observed when the associations were explored by colon and rectal cancer site (two-sided P difference = .87) and after excluding case patients diagnosed within the first four follow-up years. These novel findings provide evidence of the role of both suppressed and activated cell-mediated immunity as reflected by prediagnostic T-N concentrations in the development of CRC.
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- 2015
87. A genome-wide association study of marginal zone lymphoma shows association to the HLA region.
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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
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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.
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- 2015
88. Sex specific associations in genome wide association analysis of renal cell carcinoma
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Laskar, Ruhina S., Muller, David C., Li, Peng, Machiela, Mitchell J., Ye, Yuanqing, Gaborieau, Valerie, Foll, Matthieu, Hofmann, Jonathan N., Colli, Leandro, Sampson, Joshua N., Wang, Zhaoming, Bacq-Daian, Delphine, Boland, Anne, Abedi-Ardekani, Behnoush, Durand, Geoffroy, Le Calvez-Kelm, Florence, Robinot, Nivonirina, Blanche, Helene, Prokhortchouk, Egor, Skryabin, Konstantin G., Burdett, Laurie, Yeager, Meredith, Radojevic-Skodric, Sanja, Savic, Slavisa, Foretova, Lenka, Holcatova, Ivana, Janout, Vladimir, Mates, Dana, Rascu, Stefan, Mukeria, Anush, Zaridze, David, Bencko, Vladimir, Cybulski, Cezary, Fabianova, Eleonora, Jinga, Viorel, Lissowska, Jolanta, Lubinski, Jan, Navratilova, Marie, Rudnai, Peter, Świątkowska, Beata, Benhamou, Simone, Cancel-Tassin, Geraldine, Cussenot, Olivier, Trichopoulou, Antonia, Riboli, Elio, Overvad, Kim, Panico, Salvatore, Ljungberg, Borje, Sitaram, Raviprakash T., Giles, Graham G., Milne, Roger L, Severi, Gianluca, Bruinsma, Fiona, Fletcher, Tony, Koppova, Kvetoslava, Larsson, Susanna C., Wolk, Alicja, Banks, Rosamonde E., Selby, Peter J., Easton, Douglas F., Pharoah, Paul, Andreotti, Gabriella, Beane Freeman, Laura E, Koutros, Stella, Albanes, Demetrius, Männistö, Satu, Weinstein, Stephanie, Clark, Peter E., Edwards, Todd L., Lipworth, Loren, Carol, Hallie, Freedman, Matthew L., Pomerantz, Mark M., Cho, Eunyoung, Kraft, Peter, Preston, Mark A., Wilson, Kathryn M., Michael Gaziano, J., Sesso, Howard D., Black, Amanda, Freedman, Neal D., Huang, Wen-Yi, Anema, John G., Kahnoski, Richard J., Lane, Brian R., Noyes, Sabrina L., Petillo, David, Teh, Bin Tean, Peters, Ulrike, White, Emily, Anderson, Garnet L., Johnson, Lisa, Luo, Juhua, Chow, Wong-Ho, Moore, Lee E., Choueiri, Toni K., Wood, Christopher, Johansson, Mattias, McKay, James D., Brown, Kevin M., Rothman, Nathaniel, Lathrop, Mark G., Deleuze, Jean-Francois, Wu, Xifeng, Brennan, Paul, Chanock, Stephen J., Purdue, Mark P., and Scelo, Ghislaine
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- 2019
- Full Text
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89. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma
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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
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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.
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- 2014
90. Genome-wide Association Study Identifies Five Susceptibility Loci for Follicular Lymphoma outside the HLA Region
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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
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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.
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- 2014
91. Childhood and adulthood passive and active smoking, and the ABO group as risk factors for pancreatic cancer in women
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Vedie, Anne‐Laure, Laouali, Nasser, Gelot, Amandine, Severi, Gianluca, Boutron‐Ruault, Marie‐Christine, and Rebours, Vinciane
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Active smoking and the A blood group are associated with pancreatic adenocarcinoma (PC) risk. However, potential interactions between those risk factors and the role of passive smoking have been little investigated. We aimed to explore specific and joint associations of passive and active smoking, and effect modification by the ABO blood group in French women. The study included 96,594 women from the E3N prospective cohort, mean age: 49 years (SD 6.7). Information on active and passive smoking was reported at inclusion and throughout follow‐up. Cases were classified according to the International Classification of Diseases 10. Associations with passive and active smoking and effect modification by the ABO blood group were investigated with multivariable Cox regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI). During a 24‐year median follow‐up, 346 incident PC cases were identified. Current smoking compared with never and former smoking (HR 1.51 [95% CI 1.08–2.10]), and passive smoking in childhood compared with no childhood exposure (HR 1.47 [95% CI 1.08–2.00]) were associated with increased PC risk, but not passive exposure in adulthood (HR 1.16 [95% CI 0.91–1.47]). Exposure to both passive smoking in childhood and current smoking was associated with a stronger risk (HR 2.80 [95% CI 1.42–5.52]) than exposure to both current smoking and passive smoking only in adulthood (HR 1.68 [95% CI 1.10–2.57]) compared with neither passive nor active smoking. Associations between active smoking and PC risk were strongest in the O or B groups, while associations with passive smoking were strongest in the A or AB blood groups, but the interaction terms were not statistically significant. Both current smoking and passive smoking in childhood were associated with PC risk, with a maximal risk of current smokers exposed to passive smoking during childhood. Possible interactions between blood groups and active or passive smoking must be investigated in a larger series.
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- 2024
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- View/download PDF
92. Genetic variation at CYP3A is associated with age at menarche and breast cancer risk: a case-control study.
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Johnson, Nichola, Dudbridge, Frank, Orr, Nick, Gibson, Lorna, Jones, Michael E, Schoemaker, Minouk J, Folkerd, Elizabeth J, Haynes, Ben P, Hopper, John L, Southey, Melissa C, Dite, Gillian S, Apicella, Carmel, Schmidt, Marjanka K, Broeks, Annegien, Van't Veer, Laura J, Atsma, Femke, Muir, Kenneth, Lophatananon, Artitaya, Fasching, Peter A, Beckmann, Matthias W, Ekici, Arif B, Renner, Stefan P, Sawyer, Elinor, Tomlinson, Ian, Kerin, Michael, Miller, Nicola, Burwinkel, Barbara, Marme, Frederik, Schneeweiss, Andreas, Sohn, Christof, Guénel, Pascal, Truong, Therese, Cordina, Emilie, Menegaux, Florence, Bojesen, Stig E, Nordestgaard, Børge G, Flyger, Henrik, Milne, Roger, Zamora, M Pilar, Arias Perez, Jose Ignacio, Benitez, Javier, Bernstein, Leslie, Anton-Culver, Hoda, Ziogas, Argyrios, Clarke Dur, Christina, Brenner, Hermann, Müller, Heiko, Arndt, Volker, Dieffenbach, Aida Karina, Meindl, Alfons, Heil, Joerg, Bartram, Claus R, Schmutzler, Rita K, Brauch, Hiltrud, Justenhoven, Christina, Ko, Yon-Dschun, GENICA (Gene Environment Interaction and Breast Cancer in Germany) Network, Nevanlinna, Heli, Muranen, Taru A, Aittomäki, Kristiina, Blomqvist, Carl, Matsuo, Keitaro, Dörk, Thilo, Bogdanova, Natalia V, Antonenkova, Natalia N, Lindblom, Annika, Mannermaa, Arto, Kataja, Vesa, Kosma, Veli-Matti, Hartikainen, Jaana M, Chenevix-Trench, Georgia, Beesley, Jonathan, kConFab Investigators, Australian Ovarian Cancer Study Group, Wu, Anna H, Van den Berg, David, Tseng, Chiu-Chen, Lambrechts, Diether, Smeets, Dominiek, Neven, Patrick, Wildiers, Hans, Chang-Claude, Jenny, Rudolph, Anja, Nickels, Stefan, Flesch-Janys, Dieter, Radice, Paolo, Peterlongo, Paolo, Bonanni, Bernardo, Pensotti, Valeria, Couch, Fergus J, Olson, Janet E, Wang, Xianshu, Fredericksen, Zachary, Pankratz, Vernon S, Giles, Graham G, Severi, Gianluca, Baglietto, Laura, Haiman, Chris, Simard, Jacques, and Goldberg, Mark S
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GENICA (Gene Environment Interaction and Breast Cancer in Germany) Network ,kConFab Investigators ,Australian Ovarian Cancer Study Group ,Humans ,Breast Neoplasms ,Genetic Predisposition to Disease ,Reproductive History ,Risk Factors ,Age Factors ,Age of Onset ,Premenopause ,Menarche ,Genotype ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Middle Aged ,European Continental Ancestry Group ,Female ,Cytochrome P-450 CYP3A ,Genetic Association Studies ,Human Genome ,Aging ,Clinical Research ,Cancer ,Genetics ,Breast Cancer ,Oncology & Carcinogenesis ,Oncology and Carcinogenesis - Abstract
IntroductionWe have previously shown that a tag single nucleotide polymorphism (rs10235235), which maps to the CYP3A locus (7q22.1), was associated with a reduction in premenopausal urinary estrone glucuronide levels and a modest reduction in risk of breast cancer in women age ≤50 years.MethodsWe further investigated the association of rs10235235 with breast cancer risk in a large case control study of 47,346 cases and 47,570 controls from 52 studies participating in the Breast Cancer Association Consortium. Genotyping of rs10235235 was conducted using a custom Illumina Infinium array. Stratified analyses were conducted to determine whether this association was modified by age at diagnosis, ethnicity, age at menarche or tumor characteristics.ResultsWe confirmed the association of rs10235235 with breast cancer risk for women of European ancestry but found no evidence that this association differed with age at diagnosis. Heterozygote and homozygote odds ratios (ORs) were OR = 0.98 (95% CI 0.94, 1.01; P = 0.2) and OR = 0.80 (95% CI 0.69, 0.93; P = 0.004), respectively (P(trend) = 0.02). There was no evidence of effect modification by tumor characteristics. rs10235235 was, however, associated with age at menarche in controls (P(trend) = 0.005) but not cases (P(trend) = 0.97). Consequently the association between rs10235235 and breast cancer risk differed according to age at menarche (P(het) = 0.02); the rare allele of rs10235235 was associated with a reduction in breast cancer risk for women who had their menarche age ≥15 years (OR(het) = 0.84, 95% CI 0.75, 0.94; OR(hom) = 0.81, 95% CI 0.51, 1.30; P(trend) = 0.002) but not for those who had their menarche age ≤11 years (OR(het) = 1.06, 95% CI 0.95, 1.19, OR(hom) = 1.07, 95% CI 0.67, 1.72; P(trend) = 0.29).ConclusionsTo our knowledge rs10235235 is the first single nucleotide polymorphism to be associated with both breast cancer risk and age at menarche consistent with the well-documented association between later age at menarche and a reduction in breast cancer risk. These associations are likely mediated via an effect on circulating hormone levels.
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- 2014
93. Genome-wide association study of subtype-specific epithelial ovarian cancer risk alleles using pooled DNA.
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Walsh, Christine, Lester, Jenny, Jensen, Allan, Kjær, Susanne, Høgdall, Claus, Høgdall, Estrid, Lundvall, Lene, Sellers, Thomas, Fridley, Brooke, Goode, Ellen, Cunningham, Julie, Vierkant, Robert, Giles, Graham, Baglietto, Laura, Severi, Gianluca, Southey, Melissa, Liang, Dong, Wu, Xifeng, Lu, Karen, Hildebrandt, Michelle, Levine, Douglas, Bisogna, Maria, Schildkraut, Joellen, Iversen, Edwin, Weber, Rachel, Berchuck, Andrew, Cramer, Daniel, Terry, Kathryn, Poole, Elizabeth, Tworoger, Shelley, Bandera, Elisa, Chandran, Urmila, Orlow, Irene, Olson, Sara, Wik, Elisabeth, Salvesen, Helga, Bjorge, Line, Halle, Mari, van Altena, Anne, Aben, Katja, Kiemeney, Lambertus, Massuger, Leon, Pejovic, Tanja, Bean, Yukie, Cybulski, Cezary, Gronwald, Jacek, Lubinski, Jan, Wentzensen, Nicolas, Brinton, Louise, Lissowska, Jolanta, Garcia-Closas, Montserrat, Dicks, Ed, Dennis, Joe, Easton, Douglas, Song, Honglin, Tyrer, Jonathan, Pharoah, Paul, Eccles, Diana, Campbell, Ian, Whittemore, Alice, McGuire, Valerie, Sieh, Weiva, Rothstein, Joseph, Flanagan, James, Paul, James, Brown, Robert, Phelan, Catherine, Risch, Harvey, McLaughlin, John, Narod, Steven, Ziogas, Argyrios, Anton-Culver, Hoda, Gentry-Maharaj, Aleksandra, Menon, Usha, Gayther, Simon, Ramus, Susan, Wu, Anna, Pearce, Celeste, Pike, Malcolm, Dansonka-Mieszkowska, Agnieszka, Rzepecka, Iwona, Szafron, Lukasz, Kupryjanczyk, Jolanta, Cook, Linda, Le, Nhu, Brooks-Wilson, Angela, Earp, Madalene, Kelemen, Linda, Magliocco, Anthony, Swenerton, Kenneth, Chenevix-Trench, Georgia, Lu, Yi, Hein, Alexander, Ekici, Arif, Beckmann, Matthias, Fasching, Peter, Lambrechts, Diether, Despierre, Evelyn, Vergote, Ignace, and Lambrechts, Sandrina
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Alleles ,Carcinoma ,Ovarian Epithelial ,DNA ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Neoplasms ,Glandular and Epithelial ,Ovarian Neoplasms ,Polymorphism ,Single Nucleotide ,Quality Control - Abstract
Epithelial ovarian cancer (EOC) is a heterogeneous cancer with both genetic and environmental risk factors. Variants influencing the risk of developing the less-common EOC subtypes have not been fully investigated. We performed a genome-wide association study (GWAS) of EOC according to subtype by pooling genomic DNA from 545 cases and 398 controls of European descent, and testing for allelic associations. We evaluated for replication 188 variants from the GWAS [56 variants for mucinous, 55 for endometrioid and clear cell, 53 for low-malignant potential (LMP) serous, and 24 for invasive serous EOC], selected using pre-defined criteria. Genotypes from 13,188 cases and 23,164 controls of European descent were used to perform unconditional logistic regression under the log-additive genetic model; odds ratios (OR) and 95 % confidence intervals are reported. Nine variants tagging six loci were associated with subtype-specific EOC risk at P
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- 2014
94. Genome-wide association study identifies 25 known breast cancer susceptibility loci as risk factors for triple-negative breast cancer.
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Purrington, Kristen, Slager, Susan, Eccles, Diana, Yannoukakos, Drakoulis, Fasching, Peter, Miron, Penelope, Carpenter, Jane, Chang-Claude, Jenny, Martin, Nicholas, Montgomery, Grant, Kristensen, Vessela, Goodfellow, Paul, Tapper, William, Rafiq, Sajjad, Gerty, Susan, Durcan, Lorraine, Konstantopoulou, Irene, Fostira, Florentia, Vratimos, Athanassios, Apostolou, Paraskevi, Konstanta, Irene, Kotoula, Vassiliki, Lakis, Sotiris, Dimopoulos, Meletios, Skarlos, Dimosthenis, Pectasides, Dimitrios, Fountzilas, George, Beckmann, Matthias, Hein, Alexander, Ruebner, Matthias, Ekici, Arif, Hartmann, Arndt, Schulz-Wendtland, Ruediger, Renner, Stefan, Janni, Wolfgang, Rack, Brigitte, Scholz, Christoph, Neugebauer, Julia, Andergassen, Ulrich, Lux, Michael, Haeberle, Lothar, Clarke, Christine, Pathmanathan, Nirmala, Rudolph, Anja, Flesch-Janys, Dieter, Nickels, Stefan, Olson, Janet, Ingle, James, Olswold, Curtis, Slettedahl, Seth, Eckel-Passow, Jeanette, Anderson, S, Visscher, Daniel, Cafourek, Victoria, Sicotte, Hugues, Prodduturi, Naresh, Weiderpass, Elisabete, Bernstein, Leslie, Ivanovich, Jennifer, Giles, Graham, Baglietto, Laura, Southey, Melissa, Kosma, Veli-Matti, Fischer, Hans-Peter, Reed, Malcom, Cross, Simon, Deming-Halverson, Sandra, Shrubsole, Martha, Cai, Qiuyin, Shu, Xiao-Ou, Daly, Mary, Weaver, Joellen, Ross, Eric, Klemp, Jennifer, Sharma, Priyanka, Torres, Diana, Rüdiger, Thomas, Wölfing, Heidrun, Ulmer, Hans-Ulrich, Försti, Asta, Khoury, Thaer, Kumar, Shicha, Pilarski, Robert, Shapiro, Charles, Greco, Dario, Heikkilä, Päivi, Aittomäki, Kristiina, Blomqvist, Carl, Irwanto, Astrid, Liu, Jianjun, Pankratz, Vernon, Wang, Xianshu, Severi, Gianluca, Mannermaa, Arto, Easton, Douglas, Hall, Per, Brauch, Hiltrud, Cox, Angela, Zheng, Wei, and Godwin, Andrew
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Adult ,Aged ,Aged ,80 and over ,Case-Control Studies ,Chromosomes ,Human ,Pair 19 ,Estrogen Receptor alpha ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Middle Aged ,Polymorphism ,Single Nucleotide ,Quantitative Trait Loci ,Triple Negative Breast Neoplasms ,Young Adult - Abstract
Triple-negative (TN) breast cancer is an aggressive subtype of breast cancer associated with a unique set of epidemiologic and genetic risk factors. We conducted a two-stage genome-wide association study of TN breast cancer (stage 1: 1529 TN cases, 3399 controls; stage 2: 2148 cases, 1309 controls) to identify loci that influence TN breast cancer risk. Variants in the 19p13.1 and PTHLH loci showed genome-wide significant associations (P < 5 × 10(-) (8)) in stage 1 and 2 combined. Results also suggested a substantial enrichment of significantly associated variants among the single nucleotide polymorphisms (SNPs) analyzed in stage 2. Variants from 25 of 74 known breast cancer susceptibility loci were also associated with risk of TN breast cancer (P < 0.05). Associations with TN breast cancer were confirmed for 10 loci (LGR6, MDM4, CASP8, 2q35, 2p24.1, TERT-rs10069690, ESR1, TOX3, 19p13.1, RALY), and we identified associations with TN breast cancer for 15 additional breast cancer loci (P < 0.05: PEX14, 2q24.1, 2q31.1, ADAM29, EBF1, TCF7L2, 11q13.1, 11q24.3, 12p13.1, PTHLH, NTN4, 12q24, BRCA2, RAD51L1-rs2588809, MKL1). Further, two SNPs independent of previously reported signals in ESR1 [rs12525163 odds ratio (OR) = 1.15, P = 4.9 × 10(-) (4)] and 19p13.1 (rs1864112 OR = 0.84, P = 1.8 × 10(-) (9)) were associated with TN breast cancer. A polygenic risk score (PRS) for TN breast cancer based on known breast cancer risk variants showed a 4-fold difference in risk between the highest and lowest PRS quintiles (OR = 4.03, 95% confidence interval 3.46-4.70, P = 4.8 × 10(-) (69)). This translates to an absolute risk for TN breast cancer ranging from 0.8% to 3.4%, suggesting that genetic variation may be used for TN breast cancer risk prediction.
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- 2014
95. Genome-wide association study of subtype-specific epithelial ovarian cancer risk alleles using pooled DNA
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Earp, Madalene A, Kelemen, Linda E, Magliocco, Anthony M, Swenerton, Kenneth D, Chenevix-Trench, Georgia, Australian Cancer Study, Australian Ovarian Cancer Study Group, Lu, Yi, Hein, Alexander, Ekici, Arif B, Beckmann, Matthias W, Fasching, Peter A, Lambrechts, Diether, Despierre, Evelyn, Vergote, Ignace, Lambrechts, Sandrina, Doherty, Jennifer A, Rossing, Mary Anne, Chang-Claude, Jenny, Rudolph, Anja, Friel, Grace, Moysich, Kirsten B, Odunsi, Kunle, Sucheston-Campbell, Lara, Lurie, Galina, Goodman, Marc T, Carney, Michael E, Thompson, Pamela J, Runnebaum, Ingo B, Dürst, Matthias, Hillemanns, Peter, Dörk, Thilo, Antonenkova, Natalia, Bogdanova, Natalia, Leminen, Arto, Nevanlinna, Heli, Pelttari, Liisa M, Butzow, Ralf, Bunker, Clareann H, Modugno, Francesmary, Edwards, Robert P, Ness, Roberta B, du Bois, Andreas, Heitz, Florian, Schwaab, Ira, Harter, Philipp, Karlan, Beth Y, Walsh, Christine, Lester, Jenny, Jensen, Allan, Kjær, Susanne K, Høgdall, Claus K, Høgdall, Estrid, Lundvall, Lene, Sellers, Thomas A, Fridley, Brooke L, Goode, Ellen L, Cunningham, Julie M, Vierkant, Robert A, Giles, Graham G, Baglietto, Laura, Severi, Gianluca, Southey, Melissa C, Liang, Dong, Wu, Xifeng, Lu, Karen, Hildebrandt, Michelle AT, Levine, Douglas A, Bisogna, Maria, Schildkraut, Joellen M, Iversen, Edwin S, Weber, Rachel Palmieri, Berchuck, Andrew, Cramer, Daniel W, Terry, Kathryn L, Poole, Elizabeth M, Tworoger, Shelley S, Bandera, Elisa V, Chandran, Urmila, Orlow, Irene, Olson, Sara H, Wik, Elisabeth, Salvesen, Helga B, Bjorge, Line, Halle, Mari K, van Altena, Anne M, Aben, Katja KH, Kiemeney, Lambertus A, Massuger, Leon FAG, Pejovic, Tanja, Bean, Yukie T, Cybulski, Cezary, Gronwald, Jacek, Lubinski, Jan, Wentzensen, Nicolas, Brinton, Louise A, Lissowska, Jolanta, Garcia-Closas, Montserrat, Dicks, Ed, and Dennis, Joe
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Biological Sciences ,Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Genetics ,Rare Diseases ,Prevention ,Ovarian Cancer ,Human Genome ,Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Alleles ,Carcinoma ,Ovarian Epithelial ,DNA ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Neoplasms ,Glandular and Epithelial ,Ovarian Neoplasms ,Polymorphism ,Single Nucleotide ,Quality Control ,Australian Cancer Study ,Australian Ovarian Cancer Study Group ,Ovarian Cancer Association Consortium ,Complementary and Alternative Medicine ,Paediatrics and Reproductive Medicine ,Genetics & Heredity ,Reproductive medicine - Abstract
Epithelial ovarian cancer (EOC) is a heterogeneous cancer with both genetic and environmental risk factors. Variants influencing the risk of developing the less-common EOC subtypes have not been fully investigated. We performed a genome-wide association study (GWAS) of EOC according to subtype by pooling genomic DNA from 545 cases and 398 controls of European descent, and testing for allelic associations. We evaluated for replication 188 variants from the GWAS [56 variants for mucinous, 55 for endometrioid and clear cell, 53 for low-malignant potential (LMP) serous, and 24 for invasive serous EOC], selected using pre-defined criteria. Genotypes from 13,188 cases and 23,164 controls of European descent were used to perform unconditional logistic regression under the log-additive genetic model; odds ratios (OR) and 95 % confidence intervals are reported. Nine variants tagging six loci were associated with subtype-specific EOC risk at P
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- 2014
96. A large-scale assessment of two-way SNP interactions in breast cancer susceptibility using 46,450 cases and 42,461 controls from the breast cancer association consortium.
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Milne, Roger, Herranz, Jesús, Michailidou, Kyriaki, Dennis, Joe, Tyrer, Jonathan, Zamora, M, Arias-Perez, José, González-Neira, Anna, Pita, Guillermo, Alonso, M, Wang, Qin, Bolla, Manjeet, Czene, Kamila, Eriksson, Mikael, Humphreys, Keith, Darabi, Hatef, Li, Jingmei, Orr, Nicholas, Schoemaker, Minouk, Jakubowska, Anna, Lubinski, Jan, Jaworska-Bieniek, Katarzyna, Durda, Katarzyna, Andrulis, Irene, Knight, Julia, Glendon, Gord, Mulligan, Anna, Bojesen, Stig, Nordestgaard, Børge, Flyger, Henrik, Nevanlinna, Heli, Muranen, Taru, Aittomäki, Kristiina, Blomqvist, Carl, Chang-Claude, Jenny, Rudolph, Anja, Seibold, Petra, Flesch-Janys, Dieter, Wang, Xianshu, Olson, Janet, Vachon, Celine, Purrington, Kristen, Winqvist, Robert, Pylkäs, Katri, Jukkola-Vuorinen, Arja, Grip, Mervi, Dunning, Alison, Shah, Mitul, Guénel, Pascal, Truong, Thérèse, Sanchez, Marie, Mulot, Claire, Brenner, Hermann, Dieffenbach, Aida, Arndt, Volker, Stegmaier, Christa, Lindblom, Annika, Margolin, Sara, Hooning, Maartje, Hollestelle, Antoinette, Collée, J, Jager, Agnes, Cox, Angela, Brock, Ian, Reed, Malcolm, Devilee, Peter, Tollenaar, Robert, Seynaeve, Caroline, Haiman, Christopher, Henderson, Brian, Schumacher, Fredrick, Le Marchand, Loic, Simard, Jacques, Dumont, Martine, Soucy, Penny, Dörk, Thilo, Bogdanova, Natalia, Hamann, Ute, Försti, Asta, Rüdiger, Thomas, Ulmer, Hans-Ulrich, Fasching, Peter, Häberle, Lothar, Ekici, Arif, Beckmann, Matthias, Fletcher, Olivia, Johnson, Nichola, dos Santos Silva, Isabel, Peto, Julian, Radice, Paolo, Peterlongo, Paolo, Peissel, Bernard, Mariani, Paolo, Giles, Graham, Severi, Gianluca, Baglietto, Laura, Sawyer, Elinor, Tomlinson, Ian, Kerin, Michael, and Miller, Nicola
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Breast Neoplasms ,Case-Control Studies ,Epistasis ,Genetic ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Logistic Models ,Polymorphism ,Single Nucleotide - Abstract
Part of the substantial unexplained familial aggregation of breast cancer may be due to interactions between common variants, but few studies have had adequate statistical power to detect interactions of realistic magnitude. We aimed to assess all two-way interactions in breast cancer susceptibility between 70,917 single nucleotide polymorphisms (SNPs) selected primarily based on prior evidence of a marginal effect. Thirty-eight international studies contributed data for 46,450 breast cancer cases and 42,461 controls of European origin as part of a multi-consortium project (COGS). First, SNPs were preselected based on evidence (P < 0.01) of a per-allele main effect, and all two-way combinations of those were evaluated by a per-allele (1 d.f.) test for interaction using logistic regression. Second, all 2.5 billion possible two-SNP combinations were evaluated using Boolean operation-based screening and testing, and SNP pairs with the strongest evidence of interaction (P < 10(-4)) were selected for more careful assessment by logistic regression. Under the first approach, 3277 SNPs were preselected, but an evaluation of all possible two-SNP combinations (1 d.f.) identified no interactions at P < 10(-8). Results from the second analytic approach were consistent with those from the first (P > 10(-10)). In summary, we observed little evidence of two-way SNP interactions in breast cancer susceptibility, despite the large number of SNPs with potential marginal effects considered and the very large sample size. This finding may have important implications for risk prediction, simplifying the modelling required. Further comprehensive, large-scale genome-wide interaction studies may identify novel interacting loci if the inherent logistic and computational challenges can be overcome.
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- 2014
97. Genetic predisposition to in situ and invasive lobular carcinoma of the breast.
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Sawyer, Elinor, Roylance, Rebecca, Petridis, Christos, Brook, Mark, Nowinski, Salpie, Papouli, Efterpi, Fletcher, Olivia, Pinder, Sarah, Hanby, Andrew, Kohut, Kelly, Gorman, Patricia, Caneppele, Michele, Peto, Julian, Dos Santos Silva, Isabel, Johnson, Nichola, Swann, Ruth, Dwek, Miriam, Perkins, Katherine-Anne, Gillett, Cheryl, Houlston, Richard, Ross, Gillian, De Ieso, Paolo, Southey, Melissa, Hopper, John, Provenzano, Elena, Apicella, Carmel, Wesseling, Jelle, Cornelissen, Sten, Keeman, Renske, Fasching, Peter, Jud, Sebastian, Ekici, Arif, Beckmann, Matthias, Kerin, Michael, Marme, Federick, Schneeweiss, Andreas, Sohn, Christof, Burwinkel, Barbara, Guénel, Pascal, Truong, Therese, Laurent-Puig, Pierre, Kerbrat, Pierre, Bojesen, Stig, Nordestgaard, Børge, Nielsen, Sune, Flyger, Henrik, Milne, Roger, Perez, Jose, Menéndez, Primitiva, Benitez, Javier, Brenner, Hermann, Dieffenbach, Aida, Arndt, Volker, Stegmaier, Christa, Meindl, Alfons, Lichtner, Peter, Schmutzler, Rita, Lochmann, Magdalena, Brauch, Hiltrud, Fischer, Hans-Peter, Ko, Yon-Dschun, Nevanlinna, Heli, Muranen, Taru, Aittomäki, Kristiina, Blomqvist, Carl, Bogdanova, Natalia, Dörk, Thilo, Lindblom, Annika, Margolin, Sara, Mannermaa, Arto, Kataja, Vesa, Kosma, Veli-Matti, Hartikainen, Jaana, Chenevix-Trench, Georgia, Lambrechts, Diether, Weltens, Caroline, Van Limbergen, Erik, Hatse, Sigrid, Chang-Claude, Jenny, Rudolph, Anja, Seibold, Petra, Flesch-Janys, Dieter, Radice, Paolo, Peterlongo, Paolo, Bonanni, Bernardo, Volorio, Sara, Giles, Graham, Severi, Gianluca, Baglietto, Laura, McLean, Catriona, Haiman, Christopher, Henderson, Brian, Schumacher, Fredrick, Le Marchand, Loic, Simard, Jacques, Goldberg, Mark, Labrèche, France, Dumont, Martine, Kristensen, Vessela, and Winqvist, Robert
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Breast Neoplasms ,Carcinoma in Situ ,Carcinoma ,Lobular ,Case-Control Studies ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Genotype ,Humans ,Middle Aged ,Polymorphism ,Single Nucleotide - Abstract
Invasive lobular breast cancer (ILC) accounts for 10-15% of all invasive breast carcinomas. It is generally ER positive (ER+) and often associated with lobular carcinoma in situ (LCIS). Genome-wide association studies have identified more than 70 common polymorphisms that predispose to breast cancer, but these studies included predominantly ductal (IDC) carcinomas. To identify novel common polymorphisms that predispose to ILC and LCIS, we pooled data from 6,023 cases (5,622 ILC, 401 pure LCIS) and 34,271 controls from 36 studies genotyped using the iCOGS chip. Six novel SNPs most strongly associated with ILC/LCIS in the pooled analysis were genotyped in a further 516 lobular cases (482 ILC, 36 LCIS) and 1,467 controls. These analyses identified a lobular-specific SNP at 7q34 (rs11977670, OR (95%CI) for ILC = 1.13 (1.09-1.18), P = 6.0 × 10(-10); P-het for ILC vs IDC ER+ tumors = 1.8 × 10(-4)). Of the 75 known breast cancer polymorphisms that were genotyped, 56 were associated with ILC and 15 with LCIS at P
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- 2014
98. Risk of ovarian cancer and the NF-κB pathway: genetic association with IL1A and TNFSF10.
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Charbonneau, Bridget, Block, Matthew, Bamlet, William, Vierkant, Robert, Kalli, Kimberly, Fogarty, Zachary, Rider, David, Sellers, Thomas, Tworoger, Shelley, Poole, Elizabeth, Risch, Harvey, Salvesen, Helga, Kiemeney, Lambertus, Baglietto, Laura, Giles, Graham, Severi, Gianluca, Trabert, Britton, Wentzensen, Nicolas, Chenevix-Trench, Georgia, Whittemore, Alice, Sieh, Weiva, Chang-Claude, Jenny, Bandera, Elisa, Orlow, Irene, Terry, Kathryn, Goodman, Marc, Thompson, Pamela, Cook, Linda, Rossing, Mary, Ness, Roberta, Narod, Steven, Kupryjanczyk, Jolanta, Lu, Karen, Butzow, Ralf, Dörk, Thilo, Pejovic, Tanja, Campbell, Ian, Le, Nhu, Bunker, Clareann, Bogdanova, Natalia, Runnebaum, Ingo, Eccles, Diana, Paul, James, Wu, Anna, Gayther, Simon, Hogdall, Estrid, Heitz, Florian, Kaye, Stanley, Walsh, Christine, Despierre, Evelyn, Brinton, Louise, Hein, Alexander, Rudolph, Anja, Dansonka-Mieszkowska, Agnieszka, Olson, Sara, Harter, Philipp, Tyrer, Jonathan, Vitonis, Allison, Brooks-Wilson, Angela, Aben, Katja, Pike, Malcolm, Ramus, Susan, Wik, Elisabeth, Cybulski, Cezary, Lin, Jie, Sucheston, Lara, Edwards, Robert, McGuire, Valerie, Lester, Jenny, du Bois, Andreas, Lundvall, Lene, Wang-Gohrke, Shan, Szafron, Lukasz, Lambrechts, Sandrina, Yang, Hannah, Beckmann, Matthias, Pelttari, Liisa, Van Altena, Anne, van den Berg, David, Halle, Mari, Gentry-Maharaj, Aleksandra, Schwaab, Ira, Chandran, Urmila, Menkiszak, Janusz, Ekici, Arif, Wilkens, Lynne, Leminen, Arto, Modugno, Francesmary, Friel, Grace, Rothstein, Joseph, Vergote, Ignace, Garcia-Closas, Montserrat, Hildebrandt, Michelle, Sobiczewski, Piotr, Kelemen, Linda, Pharoah, Paul, Moysich, Kirsten, Knutson, Keith, Cunningham, Julie, and Fridley, Brooke
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Case-Control Studies ,Female ,Genetic Association Studies ,Humans ,Interleukin-1alpha ,NF-kappa B ,Ovarian Neoplasms ,Polymorphism ,Single Nucleotide ,Risk ,Signal Transduction ,TNF-Related Apoptosis-Inducing Ligand - Abstract
A missense single-nucleotide polymorphism (SNP) in the immune modulatory gene IL1A has been associated with ovarian cancer risk (rs17561). Although the exact mechanism through which this SNP alters risk of ovarian cancer is not clearly understood, rs17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian cancer. Interleukin-1α (IL1A) is both regulated by and able to activate NF-κB, a transcription factor family that induces transcription of many proinflammatory genes and may be an important mediator in carcinogenesis. We therefore tagged SNPs in more than 200 genes in the NF-κB pathway for a total of 2,282 SNPs (including rs17561) for genotype analysis of 15,604 cases of ovarian cancer in patients of European descent, including 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,016 low-grade serous, including 23,235 control cases spanning 40 studies in the Ovarian Cancer Association Consortium. In this large population, we confirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence interval (CI), 0.76-0.93; P = 0.00075], which remained intact even after excluding participants in the prior study (OR, 0.85; 95% CI, 0.75-0.95; P = 0.006). Considering a multiple-testing-corrected significance threshold of P < 2.5 × 10(-5), only one other variant, the TNFSF10 SNP rs6785617, was associated significantly with a risk of ovarian cancer (low malignant potential tumors OR, 0.85; 95% CI, 0.79-0.91; P = 0.00002). Our results extend the evidence that borderline tumors may have a distinct genetic etiology. Further investigation of how these SNPs might modify ovarian cancer associations with other inflammation-related risk factors is warranted.
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- 2014
99. Polymorphisms of an innate immune gene, toll-like receptor 4, and aggressive prostate cancer risk: a systematic review and meta-analysis.
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Weng, Pei-Hsuan, Huang, Yi-Ling, Page, John, Chen, Jen-Hau, Xu, Jianfeng, Koutros, Stella, Berndt, Sonja, Chanock, Stephen, Yeager, Meredith, Eeles, Rosalind, Easton, Douglas, Neal, David, Donovan, Jenny, Hamdy, Freddie, Muir, Kenneth, Giles, Graham, Severi, Gianluca, Smith, Jeffrey, Balistreri, Carmela, Shui, Irene, Chen, Yen-Ching, and Witte, John
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Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Immunity ,Innate ,Male ,Polymorphism ,Single Nucleotide ,Prostatic Neoplasms ,Toll-Like Receptor 4 - Abstract
BACKGROUND: Toll-like receptor 4 (TLR4) is one of the best known TLR members expressed on the surface of several leukocytes and tissue cells and has a key function in detecting pathogen and danger-associated molecular patterns. The role of TLR4 in the pathophysiology of several age-related diseases is also well recognized, such as prostate cancer (PCa). TLR4 polymorphisms have been related to PCa risk, but the relationship between TLR4 genotypes and aggressive PCa risk has not been evaluated by any systematic reviews. METHODS: We performed a systematic review and meta-analysis of candidate-gene and genome-wide association studies analyzing this relationship and included only white population. Considering appropriate criteria, only nine studies were analyzed in the meta-analysis, including 3,937 aggressive PCa and 7,382 controls. RESULTS: Using random effects model, no significant association was found in the ten TLR4 SNPs reported by at least four included studies under any inheritance model (rs2737191, rs1927914, rs10759932, rs1927911, rs11536879, rs2149356, rs4986790, rs11536889, rs7873784, and rs1554973). Pooled estimates from another ten TLR4 SNPs reported by three studies also showed no significant association (rs10759930, rs10116253, rs11536869, rs5030717, rs4986791, rs11536897, rs1927906, rs913930, rs1927905, and rs7045953). Meta-regression revealed that study type was not a significant source of between-study heterogeneity. CONCLUSIONS: TLR4 polymorphisms were not significantly associated with the risk of aggressive PCa.
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- 2014
100. Identification of New Genetic Susceptibility Loci for Breast Cancer Through Consideration of Gene‐Environment Interactions
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Schoeps, Anja, Rudolph, Anja, Seibold, Petra, Dunning, Alison M, Milne, Roger L, Bojesen, Stig E, Swerdlow, Anthony, Andrulis, Irene, Brenner, Hermann, Behrens, Sabine, Orr, Nicholas, Jones, Michael, Ashworth, Alan, Li, Jingmei, Cramp, Helen, Connley, Dan, Czene, Kamila, Darabi, Hatef, Chanock, Stephen J, Lissowska, Jolanta, Figueroa, Jonine D, Knight, Julia, Glendon, Gord, Mulligan, Anna M, Dumont, Martine, Severi, Gianluca, Baglietto, Laura, Olson, Janet, Vachon, Celine, Purrington, Kristen, Moisse, Matthieu, Neven, Patrick, Wildiers, Hans, Spurdle, Amanda, Kosma, Veli‐Matti, Kataja, Vesa, Hartikainen, Jaana M, Hamann, Ute, Ko, Yon‐Dschun, Dieffenbach, Aida K, Arndt, Volker, Stegmaier, Christa, Malats, Núria, Perez, José I Arias, Benítez, Javier, Flyger, Henrik, Nordestgaard, Børge G, Truong, Thérèse, Cordina‐Duverger, Emilie, Menegaux, Florence, dos Santos Silva, Isabel, Fletcher, Olivia, Johnson, Nichola, Häberle, Lothar, Beckmann, Matthias W, Ekici, Arif B, Braaf, Linde, Atsma, Femke, Broek, Alexandra J den, Makalic, Enes, Schmidt, Daniel F, Southey, Melissa C, Cox, Angela, Simard, Jacques, Giles, Graham G, Lambrechts, Diether, Mannermaa, Arto, Brauch, Hiltrud, Guénel, Pascal, Peto, Julian, Fasching, Peter A, Hopper, John, Flesch‐Janys, Dieter, Couch, Fergus, Chenevix‐Trench, Georgia, Pharoah, Paul DP, Garcia‐Closas, Montserrat, Schmidt, Marjanka K, Hall, Per, Easton, Douglas F, and Chang‐Claude, Jenny
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Biological Sciences ,Genetics ,Epidemiology ,Health Services and Systems ,Health Sciences ,Genetic Testing ,Human Genome ,Prevention ,Breast Cancer ,Aging ,Clinical Research ,Cancer ,Aetiology ,2.1 Biological and endogenous factors ,Adolescent ,Body Height ,Body Mass Index ,Breast Neoplasms ,Chromosomes ,Human ,Pair 21 ,Chromosomes ,Human ,Pair 6 ,Female ,Gene-Environment Interaction ,Genetic Loci ,Genetic Predisposition to Disease ,Humans ,Linkage Disequilibrium ,Menarche ,Middle Aged ,Parity ,Polymorphism ,Single Nucleotide ,Postmenopause ,White People ,breast cancer risk ,gene-environment interaction ,polymorphisms ,body mass index ,case-control study ,Public Health and Health Services - Abstract
Genes that alter disease risk only in combination with certain environmental exposures may not be detected in genetic association analysis. By using methods accounting for gene-environment (G × E) interaction, we aimed to identify novel genetic loci associated with breast cancer risk. Up to 34,475 cases and 34,786 controls of European ancestry from up to 23 studies in the Breast Cancer Association Consortium were included. Overall, 71,527 single nucleotide polymorphisms (SNPs), enriched for association with breast cancer, were tested for interaction with 10 environmental risk factors using three recently proposed hybrid methods and a joint test of association and interaction. Analyses were adjusted for age, study, population stratification, and confounding factors as applicable. Three SNPs in two independent loci showed statistically significant association: SNPs rs10483028 and rs2242714 in perfect linkage disequilibrium on chromosome 21 and rs12197388 in ARID1B on chromosome 6. While rs12197388 was identified using the joint test with parity and with age at menarche (P-values = 3 × 10(-07)), the variants on chromosome 21 q22.12, which showed interaction with adult body mass index (BMI) in 8,891 postmenopausal women, were identified by all methods applied. SNP rs10483028 was associated with breast cancer in women with a BMI below 25 kg/m(2) (OR = 1.26, 95% CI 1.15-1.38) but not in women with a BMI of 30 kg/m(2) or higher (OR = 0.89, 95% CI 0.72-1.11, P for interaction = 3.2 × 10(-05)). Our findings confirm comparable power of the recent methods for detecting G × E interaction and the utility of using G × E interaction analyses to identify new susceptibility loci.
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- 2014
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