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1. Supplementary notes from Genome-Wide Association Study of Prostate Cancer–Specific Survival

Author

Fredrik Wiklund, Sara Lindström, Johanna Schleutker, Lovise Maehle, David G. Cox, Anne Tjønneland, Bas H. Bueno-de-Mesquita, Antonia Trichopoulou, Stephanie J. Weinstein, Victoria L. Stevens, Meir J. Stampfer, Kathryn L. Penney, Alison M. Mondul, Jing Ma, Loic Le Marchand, Peter Kraft, David J. Hunter, Edward L. Giovannucci, Susan M. Gapstur, Stephen Chanock, Sonja I. Berndt, Gerald L. Andriole, Demetrius Albanes, Judith A. Clements, Jyotsna Batra, Andrzej Kierzek, Agnieszka Michael, Hardev Pandha, Sofia Maia, Paula Paulo, Manuel R. Teixeira, Amanda Spurdle, Vanio I. Mitev, Radka P. Kaneva, Chavdar Slavov, Hui-Yi Lim, Thomas A. Sellers, Jong Y. Park, Bernd Holleczek, Volker Herrmann, Hermann Brenner, Lisa Cannon-Albright, Wojciech Kluźniak, Jan Lubiński, Cezary Cybulski, Adam S. Kibel, Kathleen Herkommer, Manuel Luedeke, Walther Vogel, Christiane Maier, Daniel J. Schaid, Shannon K. McDonnell, Stephen N. Thibodeau, Janet L. Stanford, Kay-Tee Khaw, Nora Pashayan, Paul D.P. Pharoah, Freddie C. Hamdy, Jenny L. Donovan, David E. Neal, Ruth C. Travis, Timothy J. Key, Børge G. Nordestgaard, Teuvo L.J. Tammela, Csilla Sipeky, Christopher A. Haiman, Fredrick R. Schumacher, Brian E. Henderson, Liesel M. FitzGerald, Melissa C. Southey, Graham G. Giles, Kenneth Muir, Sara Benlloch, Ali Amin Al Olama, Zsofia Kote-Jarai, Douglas F. Easton, Rosalind A. Eeles, Henrik Gronberg, Markus Aly, Thomas Whitington, Robert Karlsson, and Robert Szulkin

Abstract

Supplementary acknowledgments.

Published
2023
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2. Data from Genome-Wide Association Study of Prostate Cancer–Specific Survival

Author

Fredrik Wiklund, Sara Lindström, Johanna Schleutker, Lovise Maehle, David G. Cox, Anne Tjønneland, Bas H. Bueno-de-Mesquita, Antonia Trichopoulou, Stephanie J. Weinstein, Victoria L. Stevens, Meir J. Stampfer, Kathryn L. Penney, Alison M. Mondul, Jing Ma, Loic Le Marchand, Peter Kraft, David J. Hunter, Edward L. Giovannucci, Susan M. Gapstur, Stephen Chanock, Sonja I. Berndt, Gerald L. Andriole, Demetrius Albanes, Judith A. Clements, Jyotsna Batra, Andrzej Kierzek, Agnieszka Michael, Hardev Pandha, Sofia Maia, Paula Paulo, Manuel R. Teixeira, Amanda Spurdle, Vanio I. Mitev, Radka P. Kaneva, Chavdar Slavov, Hui-Yi Lim, Thomas A. Sellers, Jong Y. Park, Bernd Holleczek, Volker Herrmann, Hermann Brenner, Lisa Cannon-Albright, Wojciech Kluźniak, Jan Lubiński, Cezary Cybulski, Adam S. Kibel, Kathleen Herkommer, Manuel Luedeke, Walther Vogel, Christiane Maier, Daniel J. Schaid, Shannon K. McDonnell, Stephen N. Thibodeau, Janet L. Stanford, Kay-Tee Khaw, Nora Pashayan, Paul D.P. Pharoah, Freddie C. Hamdy, Jenny L. Donovan, David E. Neal, Ruth C. Travis, Timothy J. Key, Børge G. Nordestgaard, Teuvo L.J. Tammela, Csilla Sipeky, Christopher A. Haiman, Fredrick R. Schumacher, Brian E. Henderson, Liesel M. FitzGerald, Melissa C. Southey, Graham G. Giles, Kenneth Muir, Sara Benlloch, Ali Amin Al Olama, Zsofia Kote-Jarai, Douglas F. Easton, Rosalind A. Eeles, Henrik Gronberg, Markus Aly, Thomas Whitington, Robert Karlsson, and Robert Szulkin

Abstract

Background: Unnecessary intervention and overtreatment of indolent disease are common challenges in clinical management of prostate cancer. Improved tools to distinguish lethal from indolent disease are critical.Methods: We performed a genome-wide survival analysis of cause-specific death in 24,023 prostate cancer patients (3,513 disease-specific deaths) from the PRACTICAL and BPC3 consortia. Top findings were assessed for replication in a Norwegian cohort (CONOR).Results: We observed no significant association between genetic variants and prostate cancer survival.Conclusions: Common genetic variants with large impact on prostate cancer survival were not observed in this study.Impact: Future studies should be designed for identification of rare variants with large effect sizes or common variants with small effect sizes. Cancer Epidemiol Biomarkers Prev; 24(11); 1796–800. ©2015 AACR.

Published
2023
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3. Prediction of Individual Genetic Risk to Prostate Cancer Using a Polygenic Score

Author

Robert, Szulkin, Thomas, Whitington, Martin, Eklund, Markus, Aly, Rosalind A, Eeles, Douglas, Easton, Z Sofia, Kote-Jarai, Ali, Amin Al Olama, Sara, Benlloch, Kenneth, Muir, Graham G, Giles, Melissa C, Southey, Liesel M, Fitzgerald, Brian E, Henderson, Fredrick, Schumacher, Christopher A, Haiman, Johanna, Schleutker, Tiina, Wahlfors, Teuvo L J, Tammela, Børge G, Nordestgaard, Tim J, Key, Ruth C, Travis, David E, Neal, Jenny L, Donovan, Freddie C, Hamdy, Paul, Pharoah, Nora, Pashayan, Kay-Tee, Khaw, Janet L, Stanford, Stephen N, Thibodeau, Shannon K, McDonnell, Daniel J, Schaid, Christiane, Maier, Walther, Vogel, Manuel, Luedeke, Kathleen, Herkommer, Adam S, Kibel, Cezary, Cybulski, Jan, Lubiński, Wojciech, Kluźniak, Lisa, Cannon-Albright, Hermann, Brenner, Katja, Butterbach, Christa, Stegmaier, Jong Y, Park, Thomas, Sellers, Hui-Yi, Lin, Hui-Yi, Lim, Chavdar, Slavov, Radka, Kaneva, Vanio, Mitev, Jyotsna, Batra, Judith A, Clements, Amanda, Spurdle, Manuel R, Teixeira, Paula, Paulo, Sofia, Maia, Hardev, Pandha, Agnieszka, Michael, Andrzej, Kierzek, Henrik, Gronberg, and Danielle M, Karyadi

Subjects
Genetic Markers, Male, Risk Factors, Genetic Variation, Humans, Prostatic Neoplasms, Genetic Predisposition to Disease, Linkage Disequilibrium, Article
Abstract

BACKGROUND. Polygenic risk scores comprising established susceptibility variants have shown to be informative classifiers for several complex diseases including prostate cancer. For prostate cancer it is unknown if inclusion of genetic markers that have so far not been associated with prostate cancer risk at a genome-wide significant level will improve disease prediction. METHODS. We built polygenic risk scores in a large training set comprising over 25,000 individuals. Initially 65 established prostate cancer susceptibility variants were selected. After LD pruning additional variants were prioritized based on their association with prostate cancer. Six-fold cross validation was performed to assess genetic risk scores and optimize the number of additional variants to be included. The final model was evaluated in an independent study population including 1,370 cases and 1,239 controls. RESULTS. The polygenic risk score with 65 established susceptibility variants provided an area under the curve (AUC) of 0.67. Adding an additional 68 novel variants significantly increased the AUC to 0.68 (P = 0.0012) and the net reclassification index with 0.21 (P = 8.5 E-08). All novel variants were located in genomic regions established as associated with prostate cancer risk. CONCLUSIONS. Inclusion of additional genetic variants from established prostate cancer susceptibility regions improves disease prediction.

Published
2015

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