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1. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa

Author

Watson, Hunna J, Yilmaz, Zeynep, Thornton, Laura M, Hübel, Christopher, Coleman, Jonathan RI, Gaspar, Héléna A, Bryois, Julien, Hinney, Anke, Leppä, Virpi M, Mattheisen, Manuel, Medland, Sarah E, Ripke, Stephan, Yao, Shuyang, Giusti-Rodríguez, Paola, Hanscombe, Ken B, Purves, Kirstin L, Adan, Roger AH, Alfredsson, Lars, Ando, Tetsuya, Andreassen, Ole A, Baker, Jessica H, Berrettini, Wade H, Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Buehren, Katharina, Burghardt, Roland, Cassina, Matteo, Cichon, Sven, Clementi, Maurizio, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, Davis, Oliver SP, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Dmitrzak-Weglarz, Monika, Docampo, Elisa, Duncan, Laramie E, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred M, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Forzan, Monica, Franklin, Christopher S, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Huckins, Laura M, Hudson, James I, Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez-Murcia, Susana, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien JH, Kennedy, James L, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Klareskog, Lars, Klump, Kelly L, Knudsen, Gun Peggy S, La Via, Maria C, Le Hellard, Stephanie, and Levitan, Robert D

Subjects
Biological Sciences, Genetics, Anorexia, Serious Mental Illness, Nutrition, Prevention, Mental Health, Clinical Research, Human Genome, Brain Disorders, Pediatric, Eating Disorders, Mental health, Adult, Anorexia Nervosa, Body Mass Index, Case-Control Studies, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genomics, Humans, Male, Mental Disorders, Metabolic Diseases, Phenotype, Prognosis, Quantitative Trait Loci, Anorexia Nervosa Genetics Initiative, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness1, affecting 0.9-4% of women and 0.3% of men2-4, with twin-based heritability estimates of 50-60%5. Mortality rates are higher than those in other psychiatric disorders6, and outcomes are unacceptably poor7. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)8,9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.

Published
2019

2. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa.

Author

Watson, Hunna J, Yilmaz, Zeynep, Thornton, Laura M, Hübel, Christopher, Coleman, Jonathan RI, Gaspar, Héléna A, Bryois, Julien, Hinney, Anke, Leppä, Virpi M, Mattheisen, Manuel, Medland, Sarah E, Ripke, Stephan, Yao, Shuyang, Giusti-Rodríguez, Paola, Anorexia Nervosa Genetics Initiative, Hanscombe, Ken B, Purves, Kirstin L, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Adan, Roger AH, Alfredsson, Lars, Ando, Tetsuya, Andreassen, Ole A, Baker, Jessica H, Berrettini, Wade H, Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Buehren, Katharina, Burghardt, Roland, Cassina, Matteo, Cichon, Sven, Clementi, Maurizio, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, Davis, Oliver SP, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Dmitrzak-Weglarz, Monika, Docampo, Elisa, Duncan, Laramie E, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred M, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Forzan, Monica, Franklin, Christopher S, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Huckins, Laura M, Hudson, James I, Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez-Murcia, Susana, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien JH, Kennedy, James L, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Klareskog, Lars, Klump, Kelly L, Knudsen, Gun Peggy S, and La Via, Maria C

Subjects
Anorexia Nervosa Genetics Initiative, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Humans, Metabolic Diseases, Genetic Predisposition to Disease, Body Mass Index, Prognosis, Case-Control Studies, Mental Disorders, Anorexia Nervosa, Genomics, Phenotype, Quantitative Trait Loci, Adult, Female, Male, Genome-Wide Association Study, Clinical Research, Mental Health, Human Genome, Nutrition, Pediatric, Prevention, Serious Mental Illness, Brain Disorders, Eating Disorders, Genetics, Anorexia, Mental health, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness1, affecting 0.9-4% of women and 0.3% of men2-4, with twin-based heritability estimates of 50-60%5. Mortality rates are higher than those in other psychiatric disorders6, and outcomes are unacceptably poor7. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)8,9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.

Published
2019

3. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa.

Author

Watson, Hunna J, Yilmaz, Zeynep, Thornton, Laura M, Hübel, Christopher, Coleman, Jonathan RI, Gaspar, Héléna A, Bryois, Julien, Hinney, Anke, Leppä, Virpi M, Mattheisen, Manuel, Medland, Sarah E, Ripke, Stephan, Yao, Shuyang, Giusti-Rodríguez, Paola, Anorexia Nervosa Genetics Initiative, Hanscombe, Ken B, Purves, Kirstin L, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Adan, Roger AH, Alfredsson, Lars, Ando, Tetsuya, Andreassen, Ole A, Baker, Jessica H, Berrettini, Wade H, Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Buehren, Katharina, Burghardt, Roland, Cassina, Matteo, Cichon, Sven, Clementi, Maurizio, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, Davis, Oliver SP, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Dmitrzak-Weglarz, Monika, Docampo, Elisa, Duncan, Laramie E, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred M, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Forzan, Monica, Franklin, Christopher S, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Huckins, Laura M, Hudson, James I, Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez-Murcia, Susana, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien JH, Kennedy, James L, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Klareskog, Lars, Klump, Kelly L, Knudsen, Gun Peggy S, and La Via, Maria C

Subjects
Anorexia Nervosa Genetics Initiative, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Humans, Metabolic Diseases, Genetic Predisposition to Disease, Body Mass Index, Prognosis, Case-Control Studies, Mental Disorders, Anorexia Nervosa, Genomics, Phenotype, Quantitative Trait Loci, Adult, Female, Male, Genome-Wide Association Study, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness1, affecting 0.9-4% of women and 0.3% of men2-4, with twin-based heritability estimates of 50-60%5. Mortality rates are higher than those in other psychiatric disorders6, and outcomes are unacceptably poor7. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)8,9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.

Published
2019

4. Recurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma

Author

Feigin, Michael E, Garvin, Tyler, Bailey, Peter, Waddell, Nicola, Chang, David K, Kelley, David R, Shuai, Shimin, Gallinger, Steven, McPherson, John D, Grimmond, Sean M, Khurana, Ekta, Stein, Lincoln D, Biankin, Andrew V, Schatz, Michael C, and Tuveson, David A

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Pancreatic Cancer, Rare Diseases, Cancer, Digestive Diseases, Adenocarcinoma, Carcinoma, Pancreatic Ductal, Gene Expression Regulation, Neoplastic, Humans, Mutation, Pancreatic Neoplasms, Receptor-Like Protein Tyrosine Phosphatases, Class 8, Sodium-Potassium-Chloride Symporters, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology, Genetics
Abstract

The contributions of coding mutations to tumorigenesis are relatively well known; however, little is known about somatic alterations in noncoding DNA. Here we describe GECCO (Genomic Enrichment Computational Clustering Operation) to analyze somatic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify commonly mutated regulatory regions. We find recurrent noncoding mutations to be enriched in PDA pathways, including axon guidance and cell adhesion, and newly identified processes, including transcription and homeobox genes. We identified mutations in protein binding sites correlating with differential expression of proximal genes and experimentally validated effects of mutations on expression. We developed an expression modulation score that quantifies the strength of gene regulation imposed by each class of regulatory elements, and found the strongest elements were most frequently mutated, suggesting a selective advantage. Our detailed single-cancer analysis of noncoding alterations identifies regulatory mutations as candidates for diagnostic and prognostic markers, and suggests new mechanisms for tumor evolution.

Published
2017

5. Recurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma.

Author

Feigin, Michael E, Garvin, Tyler, Bailey, Peter, Waddell, Nicola, Chang, David K, Kelley, David R, Shuai, Shimin, Gallinger, Steven, McPherson, John D, Grimmond, Sean M, Khurana, Ekta, Stein, Lincoln D, Biankin, Andrew V, Schatz, Michael C, and Tuveson, David A

Subjects
Humans, Adenocarcinoma, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Sodium-Potassium-Chloride Symporters, Gene Expression Regulation, Neoplastic, Mutation, Receptor-Like Protein Tyrosine Phosphatases, Class 8, Carcinoma, Pancreatic Ductal, Gene Expression Regulation, Neoplastic, Receptor-Like Protein Tyrosine Phosphatases, Class 8, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

The contributions of coding mutations to tumorigenesis are relatively well known; however, little is known about somatic alterations in noncoding DNA. Here we describe GECCO (Genomic Enrichment Computational Clustering Operation) to analyze somatic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify commonly mutated regulatory regions. We find recurrent noncoding mutations to be enriched in PDA pathways, including axon guidance and cell adhesion, and newly identified processes, including transcription and homeobox genes. We identified mutations in protein binding sites correlating with differential expression of proximal genes and experimentally validated effects of mutations on expression. We developed an expression modulation score that quantifies the strength of gene regulation imposed by each class of regulatory elements, and found the strongest elements were most frequently mutated, suggesting a selective advantage. Our detailed single-cancer analysis of noncoding alterations identifies regulatory mutations as candidates for diagnostic and prognostic markers, and suggests new mechanisms for tumor evolution.

Published
2017

6. Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer

Author

Wolpin, Brian M, Rizzato, Cosmeri, Kraft, Peter, Kooperberg, Charles, Petersen, Gloria M, Wang, Zhaoming, Arslan, Alan A, Beane-Freeman, Laura, Bracci, Paige M, Buring, Julie, Canzian, Federico, Duell, Eric J, Gallinger, Steven, Giles, Graham G, Goodman, Gary E, Goodman, Phyllis J, Jacobs, Eric J, Kamineni, Aruna, Klein, Alison P, Kolonel, Laurence N, Kulke, Matthew H, Li, Donghui, Malats, Núria, Olson, Sara H, Risch, Harvey A, Sesso, Howard D, Visvanathan, Kala, White, Emily, Zheng, Wei, Abnet, Christian C, Albanes, Demetrius, Andreotti, Gabriella, Austin, Melissa A, Barfield, Richard, Basso, Daniela, Berndt, Sonja I, Boutron-Ruault, Marie-Christine, Brotzman, Michelle, Büchler, Markus W, Bueno-de-Mesquita, H Bas, Bugert, Peter, Burdette, Laurie, Campa, Daniele, Caporaso, Neil E, Capurso, Gabriele, Chung, Charles, Cotterchio, Michelle, Costello, Eithne, Elena, Joanne, Funel, Niccola, Gaziano, J Michael, Giese, Nathalia A, Giovannucci, Edward L, Goggins, Michael, Gorman, Megan J, Gross, Myron, Haiman, Christopher A, Hassan, Manal, Helzlsouer, Kathy J, Henderson, Brian E, Holly, Elizabeth A, Hu, Nan, Hunter, David J, Innocenti, Federico, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay-Tee, Klein, Eric A, Kogevinas, Manolis, Krogh, Vittorio, Kupcinskas, Juozas, Kurtz, Robert C, LaCroix, Andrea, Landi, Maria T, Landi, Stefano, Le Marchand, Loic, Mambrini, Andrea, Mannisto, Satu, Milne, Roger L, Nakamura, Yusuke, Oberg, Ann L, Owzar, Kouros, Patel, Alpa V, Peeters, Petra HM, Peters, Ulrike, Pezzilli, Raffaele, Piepoli, Ada, Porta, Miquel, Real, Francisco X, Riboli, Elio, Rothman, Nathaniel, Scarpa, Aldo, Shu, Xiao-Ou, Silverman, Debra T, Soucek, Pavel, Sund, Malin, Talar-Wojnarowska, Renata, Taylor, Philip R, and Theodoropoulos, George E

Subjects
Cancer, Aged, Case-Control Studies, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Pancreatic Neoplasms, Polymorphism, Single Nucleotide, White People, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 × 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 × 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 × 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 × 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 × 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 × 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.

Published
2014

7. Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer.

Author

Wolpin, Brian M, Rizzato, Cosmeri, Kraft, Peter, Kooperberg, Charles, Petersen, Gloria M, Wang, Zhaoming, Arslan, Alan A, Beane-Freeman, Laura, Bracci, Paige M, Buring, Julie, Canzian, Federico, Duell, Eric J, Gallinger, Steven, Giles, Graham G, Goodman, Gary E, Goodman, Phyllis J, Jacobs, Eric J, Kamineni, Aruna, Klein, Alison P, Kolonel, Laurence N, Kulke, Matthew H, Li, Donghui, Malats, Núria, Olson, Sara H, Risch, Harvey A, Sesso, Howard D, Visvanathan, Kala, White, Emily, Zheng, Wei, Abnet, Christian C, Albanes, Demetrius, Andreotti, Gabriella, Austin, Melissa A, Barfield, Richard, Basso, Daniela, Berndt, Sonja I, Boutron-Ruault, Marie-Christine, Brotzman, Michelle, Büchler, Markus W, Bueno-de-Mesquita, H Bas, Bugert, Peter, Burdette, Laurie, Campa, Daniele, Caporaso, Neil E, Capurso, Gabriele, Chung, Charles, Cotterchio, Michelle, Costello, Eithne, Elena, Joanne, Funel, Niccola, Gaziano, J Michael, Giese, Nathalia A, Giovannucci, Edward L, Goggins, Michael, Gorman, Megan J, Gross, Myron, Haiman, Christopher A, Hassan, Manal, Helzlsouer, Kathy J, Henderson, Brian E, Holly, Elizabeth A, Hu, Nan, Hunter, David J, Innocenti, Federico, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay-Tee, Klein, Eric A, Kogevinas, Manolis, Krogh, Vittorio, Kupcinskas, Juozas, Kurtz, Robert C, LaCroix, Andrea, Landi, Maria T, Landi, Stefano, Le Marchand, Loic, Mambrini, Andrea, Mannisto, Satu, Milne, Roger L, Nakamura, Yusuke, Oberg, Ann L, Owzar, Kouros, Patel, Alpa V, Peeters, Petra HM, Peters, Ulrike, Pezzilli, Raffaele, Piepoli, Ada, Porta, Miquel, Real, Francisco X, Riboli, Elio, Rothman, Nathaniel, Scarpa, Aldo, Shu, Xiao-Ou, Silverman, Debra T, Soucek, Pavel, Sund, Malin, Talar-Wojnarowska, Renata, Taylor, Philip R, and Theodoropoulos, George E

Subjects
Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Genotype, Polymorphism, Single Nucleotide, Aged, Middle Aged, European Continental Ancestry Group, Female, Male, Genome-Wide Association Study, Genetic Loci, Polymorphism, Single Nucleotide, Medical And Health Sciences, Biological Sciences, Developmental Biology, Medical and Health Sciences
Abstract

We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 × 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 × 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 × 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 × 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 × 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 × 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.

Published
2014

8. A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.

Author

Petersen, Gloria M, Amundadottir, Laufey, Fuchs, Charles S, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Jacobs, Kevin B, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gallinger, Steven, Gross, Myron, Helzlsouer, Kathy, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, LaCroix, Andrea, Li, Donghui, Mandelson, Margaret T, Olson, Sara H, Risch, Harvey A, Zheng, Wei, Albanes, Demetrius, Bamlet, William R, Berg, Christine D, Boutron-Ruault, Marie-Christine, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Howard, Barbara, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Kaaks, Rudolf, Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C, Lynch, Shannon M, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Parikh, Hemang, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Rodriguez, Laudina, Seminara, Daniela, Shu, Xiao-Ou, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wang, Zhaoming, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Fraumeni, Joseph F, Hoover, Robert N, Hartge, Patricia, and Chanock, Stephen J

Subjects
Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 13, Humans, Carcinoma, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Loci, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.

Published
2010

9. A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.

Author

Petersen, Gloria M, Amundadottir, Laufey, Fuchs, Charles S, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Jacobs, Kevin B, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gallinger, Steven, Gross, Myron, Helzlsouer, Kathy, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, LaCroix, Andrea, Li, Donghui, Mandelson, Margaret T, Olson, Sara H, Risch, Harvey A, Zheng, Wei, Albanes, Demetrius, Bamlet, William R, Berg, Christine D, Boutron-Ruault, Marie-Christine, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Howard, Barbara, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Kaaks, Rudolf, Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C, Lynch, Shannon M, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Parikh, Hemang, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Rodriguez, Laudina, Seminara, Daniela, Shu, Xiao-Ou, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wang, Zhaoming, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Fraumeni, Joseph F, Hoover, Robert N, Hartge, Patricia, and Chanock, Stephen J

Subjects
Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 13, Humans, Carcinoma, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Loci, Human Genome, Cancer, Rare Diseases, Clinical Research, Pancreatic Cancer, Digestive Diseases, Genetics, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.

Published
2010

10. Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer.

Author

Amundadottir, Laufey, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Fuchs, Charles S, Petersen, Gloria M, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Zheng, Wei, Albanes, Demetrius, Bamlet, William, Berg, Christine D, Berrino, Franco, Bingham, Sheila, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clavel-Chapelon, Françoise, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Fox, John W, Gallinger, Steven, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, González, Carlos A, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Holly, Elizabeth A, Hunter, David J, Hutchinson, Amy, Jackson, Rebecca, Jacobs, Kevin B, Jenab, Mazda, Kaaks, Rudolf, Klein, Alison P, Kooperberg, Charles, Kurtz, Robert C, Li, Donghui, Lynch, Shannon M, Mandelson, Margaret, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Olson, Sara H, Overvad, Kim, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Risch, Harvey A, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Chanock, Stephen J, Hartge, Patricia, and Hoover, Robert N

Subjects
Chromosomes, Human, Pair 9, Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, ABO Blood-Group System, Logistic Models, Odds Ratio, Risk Factors, Case-Control Studies, Cohort Studies, Prospective Studies, Gene Frequency, Genotype, Haplotypes, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Alleles, Introns, United States, Female, Male, Genetic Variation, Genome-Wide Association Study, Prevention, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.

Published
2009

11. Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer.

Author

Amundadottir, Laufey, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Fuchs, Charles S, Petersen, Gloria M, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Zheng, Wei, Albanes, Demetrius, Bamlet, William, Berg, Christine D, Berrino, Franco, Bingham, Sheila, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clavel-Chapelon, Françoise, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Fox, John W, Gallinger, Steven, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, González, Carlos A, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Holly, Elizabeth A, Hunter, David J, Hutchinson, Amy, Jackson, Rebecca, Jacobs, Kevin B, Jenab, Mazda, Kaaks, Rudolf, Klein, Alison P, Kooperberg, Charles, Kurtz, Robert C, Li, Donghui, Lynch, Shannon M, Mandelson, Margaret, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Olson, Sara H, Overvad, Kim, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Risch, Harvey A, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Chanock, Stephen J, Hartge, Patricia, and Hoover, Robert N

Subjects
Chromosomes, Human, Pair 9, Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, ABO Blood-Group System, Logistic Models, Odds Ratio, Risk Factors, Case-Control Studies, Cohort Studies, Prospective Studies, Gene Frequency, Genotype, Haplotypes, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Alleles, Introns, United States, Female, Male, Genetic Variation, Genome-Wide Association Study, Human Genome, Genetics, Clinical Research, Pancreatic Cancer, Prevention, Digestive Diseases, Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.

Published
2009

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