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1. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysisResearch in context

Author: James Yarmolinsky, Jamie W. Robinson, Daniela Mariosa, Ville Karhunen, Jian Huang, Niki Dimou, Neil Murphy, Kimberley Burrows, Emmanouil Bouras, Karl Smith-Byrne, Sarah J. Lewis, Tessel E. Galesloot, Lambertus A. Kiemeney, Sita Vermeulen, Paul Martin, Demetrius Albanes, Lifang Hou, Polly A. Newcomb, Emily White, Alicja Wolk, Anna H. Wu, Loïc Le Marchand, Amanda I. Phipps, Daniel D. Buchanan, Sizheng Steven Zhao, Dipender Gill, Stephen J. Chanock, Mark P. Purdue, George Davey Smith, Paul Brennan, Karl-Heinz Herzig, Marjo-Riitta Järvelin, Chris I. Amos, Rayjean J. Hung, Abbas Dehghan, Mattias Johansson, Marc J. Gunter, Kostas K. Tsilidis, Richard M. Martin, Maria Teresa Landi, Victoria Stevens, Ying Wang, Demetrios Albanes, Neil Caporaso, Christopher I. Amos, Sanjay Shete, Heike Bickeböller, Angela Risch, Richard Houlston, Stephen Lam, Adonina Tardon, Chu Chen, Stig E. Bojesen, H-Erich Wichmann, David Christiani, Gadi Rennert, Susanne Arnold, John K. Field, Loic Le Marchand, Olle Melander, Hans Brunnström, Geoffrey Liu, Angeline Andrew, Hongbing Shen, Shan Zienolddiny, Kjell Grankvist, Mikael Johansson, M. Dawn Teare, Yun-Chul Hong, Jian-Min Yuan, Philip Lazarus, Matthew B. Schabath, Melinda C. Aldrich, Rosalind A. Eeles, Christopher A. Haiman, Zsofia Kote-Jarai, Fredrick R. Schumacher, Sara Benlloch, Ali Amin Al Olama, Kenneth R. Muir, Sonja I. Berndt, David V. Conti, Fredrik Wiklund, Stephen Chanock, Catherine M. Tangen, Jyotsna Batra, Judith A. Clements, Henrik Grönberg, Nora Pashayan, Johanna Schleutker, Stephanie J. Weinstein, Catharine M.L. West, Lorelei A. Mucci, Géraldine Cancel-Tassin, Stella Koutros, Karina Dalsgaard Sørensen, Eli Marie Grindedal, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Sue Ann Ingles, Barry S. Rosenstein, Yong-Jie Lu, Graham G. Giles, Robert J. MacInnis, Adam S. Kibel, Ana Vega, Manolis Kogevinas, Kathryn L. Penney, Jong Y. Park, Janet L. Stanfrod, Cezary Cybulski, Børge G. Nordestgaard, Sune F. Nielsen, Hermann Brenner, Christiane Maier, Christopher J. Logothetis, Esther M. John, Manuel R. Teixeira, Susan L. Neuhausen, Kim De Ruyck, Azad Razack, Lisa F. Newcomb, Davor Lessel, Radka Kaneva, Nawaid Usmani, Frank Claessens, Paul A. Townsend, Jose Esteban Castelao, Monique J. Roobol, Florence Menegaux, Kay-Tee Khaw, Lisa Cannon-Albright, Hardev Pandha, Stephen N. Thibodeau, David J. Hunter, Peter Kraft, William J. Blot, and Elio Riboli
Subjects: Inflammation, Cancer, Mendelian randomization, Genetic epidemiology, Medicine, Medicine (General), R5-920
Abstract: Summary: Background: Tumour-promoting inflammation is a “hallmark” of cancer and conventional epidemiological studies have reported links between various inflammatory markers and cancer risk. The causal nature of these relationships and, thus, the suitability of these markers as intervention targets for cancer prevention is unclear. Methods: We meta-analysed 6 genome-wide association studies of circulating inflammatory markers comprising 59,969 participants of European ancestry. We then used combined cis-Mendelian randomization and colocalisation analysis to evaluate the causal role of 66 circulating inflammatory markers in risk of 30 adult cancers in 338,294 cancer cases and up to 1,238,345 controls. Genetic instruments for inflammatory markers were constructed using genome-wide significant (P 70% was employed to indicate support for shared causal variants across inflammatory markers and cancer outcomes. Findings were replicated in the FinnGen study and then pooled using meta-analysis. Findings: We found strong evidence to support an association of genetically-proxied circulating pro-adrenomedullin concentrations with increased breast cancer risk (OR: 1.19, 95% CI: 1.10–1.29, q-value = 0.033, PPH4 = 84.3%) and suggestive evidence to support associations of interleukin-23 receptor concentrations with increased pancreatic cancer risk (OR: 1.42, 95% CI: 1.20–1.69, q-value = 0.055, PPH4 = 73.9%), prothrombin concentrations with decreased basal cell carcinoma risk (OR: 0.66, 95% CI: 0.53–0.81, q-value = 0.067, PPH4 = 81.8%), and interleukin-1 receptor-like 1 concentrations with decreased triple-negative breast cancer risk (OR: 0.92, 95% CI: 0.88–0.97, q-value = 0.15, PPH4 = 85.6%). These findings were replicated in pooled analyses with the FinnGen study. Though suggestive evidence was found to support an association of macrophage migration inhibitory factor concentrations with increased bladder cancer risk (OR: 2.46, 95% CI: 1.48–4.10, q-value = 0.072, PPH4 = 76.1%), this finding was not replicated when pooled with the FinnGen study. For 22 of 30 cancer outcomes examined, there was little evidence (q-value ≥0.20) that any of the 66 circulating inflammatory markers examined were associated with cancer risk. Interpretation: Our comprehensive joint Mendelian randomization and colocalisation analysis of the role of circulating inflammatory markers in cancer risk identified potential roles for 4 circulating inflammatory markers in risk of 4 site-specific cancers. Contrary to reports from some prior conventional epidemiological studies, we found little evidence of association of circulating inflammatory markers with the majority of site-specific cancers evaluated. Funding: Cancer Research UK (C68933/A28534, C18281/A29019, PPRCPJT∖100005), World Cancer Research Fund (IIG_FULL_2020_022), National Institute for Health Research (NIHR202411, BRC-1215-20011), Medical Research Council (MC_UU_00011/1, MC_UU_00011/3, MC_UU_00011/6, and MC_UU_00011/4), Academy of Finland Project 326291, European Union's Horizon 2020 grant agreement no. 848158 (EarlyCause), French National Cancer Institute (INCa SHSESP20, 2020-076), Versus Arthritis (21173, 21754, 21755), National Institutes of Health (U19 CA203654), National Cancer Institute (U19CA203654).
Published: 2024
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2. Sexually and non‐sexually transmitted infections and the risk of prostate cancer: Results from the EPICAP study

Author: Melissa Sawaya, Emilie Cordina‐Duverger, Pierre‐Jean Lamy, Xavier Rébillard, Brigitte Trétarre, and Florence Menegaux
Subjects: cancer prevention, cancer risk factors, epidemiology, prostate cancer, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Abstract Introduction Prostate cancer (PCa) is by far the most common type of cancer among men in western countries. However, relatively little is known about its etiology despite the high morbidity and mortality. It has been suggested that chronic inflammation may be involved in prostate carcinogenesis. We investigated the role of sexually and non‐sexually transmitted infections in prostate cancer risk with a specific interest in the aggressive types. Methods We used data from epidemiological study of prostate cancer (EPICAP), a population‐based case–control study. A total of 819 incident cases and 879 controls were interviewed face‐to‐face using a standardized questionnaire gathering information on known or suspected risk factors of prostate cancer and personal history of specific sexually and non‐sexually transmitted infections: gonorrhea, syphilis, trichomonas, herpes, mononucleosis, Epstein–Barr virus, varicella‐zoster, and dengue. Odds ratios (OR) and their 95% confidence interval were estimated using multivariate unconditional logistic regression. Results There was no significant association between gonorrhea (OR: 0.90, 95% CI: 0.61–1.33), trichomonas (OR: 0.74, 95% CI: 0.27–2.07), genital herpes (OR: 0.69, 95% CI: 0.38–1.27), and the risk of prostate cancer. No association emerged for overall sexually transmitted bacterial and viral infections (OR 1.05, 95% CI: 0.86–1.29) and overall non‐sexually transmitted viral infections (OR 1.11, 95% CI: 0.90–1.35) and the risk of prostate cancer. Conclusion Our results showed that sexually or non‐sexually transmitted infections, either bacterial or viral, were not associated to prostate cancer. Therefore, further investigation is needed to help advance our understanding of the role of chronic inflammation in the etiology of prostate cancer, with a particular focus on its most aggressive types.
Published: 2024
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3. Pre-diagnostic C-reactive protein concentrations, CRP genetic variation and mortality among individuals with colorectal cancer in Western European populations

Author: Katharina Nimptsch, Krasimira Aleksandrova, Veronika Fedirko, Mazda Jenab, Marc J. Gunter, Peter D. Siersema, Kana Wu, Verena Katzke, Rudolf Kaaks, Salvatore Panico, Domenico Palli, Anne M May, Sabina Sieri, Bas Bueno-de-Mesquita, Karina Standahl, Maria-Jose Sánchez, Aurora Perez-Cornago, Anja Olsen, Anne Tjønneland, Catalina Bonet Bonet, Christina C. Dahm, María-Dolores Chirlaque, Valentina Fiano, Rosario Tumino, Aurelio Barricarte Gurrea, Marie-Christine Boutron-Ruault, Florence Menegaux, Gianluca Severi, Bethany van Guelpen, Young-Ae Lee, and Tobias Pischon
Subjects: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Abstract Background The role of elevated pre-diagnostic C-reactive protein (CRP) concentrations on mortality in individuals with colorectal cancer (CRC) remains unclear. Methods We investigated the association between pre-diagnostic high-sensitivity CRP concentrations and CRP genetic variation associated with circulating CRP and CRC-specific and all-cause mortality based on data from 1,235 individuals with CRC within the European Prospective Investigation into Cancer and Nutrition cohort using multivariable-adjusted Cox proportional hazards regression. Results During a median follow-up of 9.3 years, 455 CRC-specific deaths were recorded, out of 590 deaths from all causes. Pre-diagnostic CRP concentrations were not associated with CRC-specific (hazard ratio, HR highest versus lowest quintile 0.92, 95% confidence interval, CI 0.66, 1.28) or all-cause mortality (HR 0.91, 95% CI 0.68, 1.21). Genetic predisposition to higher CRP (weighted score based on alleles of four CRP SNPs associated with higher circulating CRP) was not significantly associated with CRC-specific mortality (HR per CRP-score unit 0.95, 95% CI 0.86, 1.05) or all-cause mortality (HR 0.98, 95% CI 0.90, 1.07). Among four investigated CRP genetic variants, only SNP rs1205 was significantly associated with CRC-specific (comparing the CT and CC genotypes with TT genotype, HR 0.54, 95% CI 0.35, 0.83 and HR 0.58, 95% CI 0.38, 0.88, respectively) and all-cause mortality (HR 0.58, 95% CI 0.40, 0.85 and 0.64, 95% CI 0.44, 0.92, respectively). Conclusions The results of this prospective cohort study do not support a role of pre-diagnostic CRP concentrations on mortality in individuals with CRC. The observed associations with rs1205 deserve further scientific attention.
Published: 2022
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4. Occupation and prostate Cancer risk: results from the epidemiological study of prostate cancer (EPICAP)

Author: Wendy Bijoux, Emilie Cordina-Duverger, Soumaya Balbolia, Pierre-Jean Lamy, Xavier Rebillard, Brigitte Tretarre, Sylvie Cenee, and Florence Menegaux
Subjects: Prostate cancer, Aggressive prostate cancer, Occupation, Case-control study, Industrial medicine. Industrial hygiene, RC963-969
Abstract: Abstract Background Although prostate cancer (PCa) is the most frequent male cancer in industrialized countries, little is known about its aetiology. The literature has suggested an influence of the environment, including occupational exposures, but results are inconsistent. In this context, we investigated PCa risk associated to employment among several occupations using data from EPICAP study. Methods EPICAP is a French population-based case-control study including 819 PCa incident cases and 879 controls frequency-matched on age. In-person interviews gathered data on potential risk factors and lifetime occupational histories for each job held at least 6 months. Then, occupations were coded using ISCO 68. Unconditional logistic regressions were performed to assess the association between occupations (ever occupied and by duration) and PCa risk, whether all and aggressive, after adjusting for potential confounders. Results For ≥10 years of employment, we found positive associations with PCa, whether overall and aggressive, among Medical, Dental and Veterinary workers (OR (odds ratios) =5.01 [95% confidence interval] [1.27; 19.77]), Members of the armed forces (OR = 5.14 [0.99; 26.71]) and Fishermen, hunters and related workers (OR = 4.58 [1.33; 15.78]); whether overall and non-aggressive PCa, among Legislative officials and Government administrators (OR = 3.30 [1.10; 9.84]) or Managers (OR = 1.68 [1.18; 2.41]); however a negative association, whether overall and non-aggressive PCa, among Material-Handling and Related Equipment Operators, Dockers and Freight Handlers (OR = 0.40 [0.17; 0.97]). Conclusion Excess PCa risks were observed in the EPICAP study mostly among white collar workers exposed to several factors in their work environment. These emerging associations can be used to lead future research investigating specific occupational exposures.
Published: 2022
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5. Polygenic hazard score is associated with prostate cancer in multi-ethnic populations

Author: Minh-Phuong Huynh-Le, Chun Chieh Fan, Roshan Karunamuni, Wesley K. Thompson, Maria Elena Martinez, Rosalind A. Eeles, Zsofia Kote-Jarai, Kenneth Muir, Johanna Schleutker, Nora Pashayan, Jyotsna Batra, Henrik Grönberg, David E. Neal, Jenny L. Donovan, Freddie C. Hamdy, Richard M. Martin, Sune F. Nielsen, Børge G. Nordestgaard, Fredrik Wiklund, Catherine M. Tangen, Graham G. Giles, Alicja Wolk, Demetrius Albanes, Ruth C. Travis, William J. Blot, Wei Zheng, Maureen Sanderson, Janet L. Stanford, Lorelei A. Mucci, Catharine M. L. West, Adam S. Kibel, Olivier Cussenot, Sonja I. Berndt, Stella Koutros, Karina Dalsgaard Sørensen, Cezary Cybulski, Eli Marie Grindedal, Florence Menegaux, Kay-Tee Khaw, Jong Y. Park, Sue A. Ingles, Christiane Maier, Robert J. Hamilton, Stephen N. Thibodeau, Barry S. Rosenstein, Yong-Jie Lu, Stephen Watya, Ana Vega, Manolis Kogevinas, Kathryn L. Penney, Chad Huff, Manuel R. Teixeira, Luc Multigner, Robin J. Leach, Lisa Cannon-Albright, Hermann Brenner, Esther M. John, Radka Kaneva, Christopher J. Logothetis, Susan L. Neuhausen, Kim De Ruyck, Hardev Pandha, Azad Razack, Lisa F. Newcomb, Jay H. Fowke, Marija Gamulin, Nawaid Usmani, Frank Claessens, Manuela Gago-Dominguez, Paul A. Townsend, William S. Bush, Monique J. Roobol, Marie-Élise Parent, Jennifer J. Hu, Ian G. Mills, Ole A. Andreassen, Anders M. Dale, Tyler M. Seibert, UKGPCS collaborators, APCB (Australian Prostate Cancer BioResource), NC-LA PCaP Investigators, The IMPACT Study Steering Committee and Collaborators, Canary PASS Investigators, The Profile Study Steering Committee, and The PRACTICAL Consortium
Subjects: Science
Abstract: A polygenic hazard score (PHS1) improves prostate cancer screening accuracy in European patients. Here, the authors test the performance of a version compatible with OncoArray genotypes (PHS2) in a multi-ethnic dataset and find that it risk-stratifies men for any, aggressive, and fatal prostate cancer.
Published: 2021
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6. Body mass index trajectories and prostate cancer risk: Results from the EPICAP study

Author: Céline Lavalette, Emilie Cordina Duverger, Fanny Artaud, Xavier Rébillard, Pierre‐Jean Lamy, Brigitte Trétarre, Sylvie Cénée, and Florence Menegaux
Subjects: body mass index, obesity, prostate cancer, trajectory, weight gain, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Abstract Elevated body mass index (BMI) has been inconsistently associated with prostate cancer occurrence but it has been suggested that life course adulthood obesity may be associated with an increased risk of prostate cancer. However, few studies have investigated lifetime BMI and prostate cancer risk. We analyzed life course BMI trajectories on prostate cancer risk based on data from the Epidemiological study of Prostate Cancer (EPICAP). We included in our analyses 781 incident prostate cancer cases and 829 controls frequency matched by age. Participants were asked about their weight every decade from age 20 to two years before reference date. BMI trajectories were determined using group‐based trajectory modeling to identify groups of men with similar patterns of BMI changes. We identified five BMI trajectories groups. Men with a normal BMI at age 20 developing overweight or obesity during adulthood were at increased risk of aggressive prostate cancer compared to men who maintained a normal BMI. Our results suggest that BMI trajectories resulting in overweight or obesity during adulthood are associated with an increased risk of aggressive prostate cancer, particularly in never smokers, emphasizing the importance of maintaining a healthy BMI throughout adulthood.
Published: 2020
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7. Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author: Marco Matejcic, Edward J. Saunders, Tokhir Dadaev, Mark N. Brook, Kan Wang, Xin Sheng, Ali Amin Al Olama, Fredrick R. Schumacher, Sue A. Ingles, Koveela Govindasami, Sara Benlloch, Sonja I. Berndt, Demetrius Albanes, Stella Koutros, Kenneth Muir, Victoria L. Stevens, Susan M. Gapstur, Catherine M. Tangen, Jyotsna Batra, Judith Clements, Henrik Gronberg, Nora Pashayan, Johanna Schleutker, Alicja Wolk, Catharine West, Lorelei Mucci, Peter Kraft, Géraldine Cancel-Tassin, Karina D. Sorensen, Lovise Maehle, Eli M. Grindedal, Sara S. Strom, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Barry Rosenstein, Yong-Jie Lu, Graham G. Giles, Adam S. Kibel, Ana Vega, Jeanette T. Bensen, Manolis Kogevinas, Kathryn L. Penney, Jong Y. Park, Janet L. Stanford, Cezary Cybulski, Børge G. Nordestgaard, Hermann Brenner, Christiane Maier, Jeri Kim, Manuel R. Teixeira, Susan L. Neuhausen, Kim De Ruyck, Azad Razack, Lisa F. Newcomb, Davor Lessel, Radka Kaneva, Nawaid Usmani, Frank Claessens, Paul A. Townsend, Manuela Gago-Dominguez, Monique J. Roobol, Florence Menegaux, Kay-Tee Khaw, Lisa A. Cannon-Albright, Hardev Pandha, Stephen N. Thibodeau, Daniel J. Schaid, The PRACTICAL Consortium, Fredrik Wiklund, Stephen J. Chanock, Douglas F. Easton, Rosalind A. Eeles, Zsofia Kote-Jarai, David V. Conti, and Christopher A. Haiman
Subjects: Science
Abstract: The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.
Published: 2019
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8. Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author: Marco Matejcic, Edward J. Saunders, Tokhir Dadaev, Mark N. Brook, Kan Wang, Xin Sheng, Ali Amin Al Olama, Fredrick R. Schumacher, Sue A. Ingles, Koveela Govindasami, Sara Benlloch, Sonja I. Berndt, Demetrius Albanes, Stella Koutros, Kenneth Muir, Victoria L. Stevens, Susan M. Gapstur, Catherine M. Tangen, Jyotsna Batra, Judith Clements, Henrik Gronberg, Nora Pashayan, Johanna Schleutker, Alicja Wolk, Catharine West, Lorelei Mucci, Peter Kraft, Géraldine Cancel-Tassin, Karina D. Sorensen, Lovise Maehle, Eli M. Grindedal, Sara S. Strom, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Barry Rosenstein, Yong-Jie Lu, Graham G. Giles, Adam S. Kibel, Ana Vega, Jeanette T. Bensen, Manolis Kogevinas, Kathryn L. Penney, Jong Y. Park, Janet L. Stanford, Cezary Cybulski, Børge G. Nordestgaard, Hermann Brenner, Christiane Maier, Jeri Kim, Manuel R. Teixeira, Susan L. Neuhausen, Kim De Ruyck, Azad Razack, Lisa F. Newcomb, Davor Lessel, Radka Kaneva, Nawaid Usmani, Frank Claessens, Paul A. Townsend, Manuela Gago-Dominguez, Monique J. Roobol, Florence Menegaux, Kay-Tee Khaw, Lisa A. Cannon-Albright, Hardev Pandha, Stephen N. Thibodeau, Daniel J. Schaid, The PRACTICAL (Prostate Cancer Association Group to Investigate Cancer-Associated Alterations in the Genome) Consortium, Fredrik Wiklund, Stephen J. Chanock, Douglas F. Easton, Rosalind A. Eeles, Zsofia Kote-Jarai, David V. Conti, and Christopher A. Haiman
Subjects: Science
Abstract: Chromosome 8q24 is known to be a major susceptibility region for prostate cancer risk. Here the authors analyze genetic data across the 8q24 region from 71,535 prostate cancer patients identifying 12 risk loci, three previously unreported, highlighting the contribution of germline variation at this locus.
Published: 2018
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9. Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Author: Tokhir Dadaev, Edward J. Saunders, Paul J. Newcombe, Ezequiel Anokian, Daniel A. Leongamornlert, Mark N. Brook, Clara Cieza-Borrella, Martina Mijuskovic, Sarah Wakerell, Ali Amin Al Olama, Fredrick R. Schumacher, Sonja I. Berndt, Sara Benlloch, Mahbubl Ahmed, Chee Goh, Xin Sheng, Zhuo Zhang, Kenneth Muir, Koveela Govindasami, Artitaya Lophatananon, Victoria L. Stevens, Susan M. Gapstur, Brian D. Carter, Catherine M. Tangen, Phyllis Goodman, Ian M. Thompson, Jyotsna Batra, Suzanne Chambers, Leire Moya, Judith Clements, Lisa Horvath, Wayne Tilley, Gail Risbridger, Henrik Gronberg, Markus Aly, Tobias Nordström, Paul Pharoah, Nora Pashayan, Johanna Schleutker, Teuvo L. J. Tammela, Csilla Sipeky, Anssi Auvinen, Demetrius Albanes, Stephanie Weinstein, Alicja Wolk, Niclas Hakansson, Catharine West, Alison M. Dunning, Neil Burnet, Lorelei Mucci, Edward Giovannucci, Gerald Andriole, Olivier Cussenot, Géraldine Cancel-Tassin, Stella Koutros, Laura E. Beane Freeman, Karina Dalsgaard Sorensen, Torben Falck Orntoft, Michael Borre, Lovise Maehle, Eli Marie Grindedal, David E. Neal, Jenny L. Donovan, Freddie C. Hamdy, Richard M. Martin, Ruth C. Travis, Tim J. Key, Robert J. Hamilton, Neil E. Fleshner, Antonio Finelli, Sue Ann Ingles, Mariana C. Stern, Barry Rosenstein, Sarah Kerns, Harry Ostrer, Yong-Jie Lu, Hong-Wei Zhang, Ninghan Feng, Xueying Mao, Xin Guo, Guomin Wang, Zan Sun, Graham G. Giles, Melissa C. Southey, Robert J. MacInnis, Liesel M. FitzGerald, Adam S. Kibel, Bettina F. Drake, Ana Vega, Antonio Gómez-Caamaño, Laura Fachal, Robert Szulkin, Martin Eklund, Manolis Kogevinas, Javier Llorca, Gemma Castaño-Vinyals, Kathryn L. Penney, Meir Stampfer, Jong Y. Park, Thomas A. Sellers, Hui-Yi Lin, Janet L. Stanford, Cezary Cybulski, Dominika Wokolorczyk, Jan Lubinski, Elaine A. Ostrander, Milan S. Geybels, Børge G. Nordestgaard, Sune F. Nielsen, Maren Weisher, Rasmus Bisbjerg, Martin Andreas Røder, Peter Iversen, Hermann Brenner, Katarina Cuk, Bernd Holleczek, Christiane Maier, Manuel Luedeke, Thomas Schnoeller, Jeri Kim, Christopher J. Logothetis, Esther M. John, Manuel R. Teixeira, Paula Paulo, Marta Cardoso, Susan L. Neuhausen, Linda Steele, Yuan Chun Ding, Kim De Ruyck, Gert De Meerleer, Piet Ost, Azad Razack, Jasmine Lim, Soo-Hwang Teo, Daniel W. Lin, Lisa F. Newcomb, Davor Lessel, Marija Gamulin, Tomislav Kulis, Radka Kaneva, Nawaid Usmani, Chavdar Slavov, Vanio Mitev, Matthew Parliament, Sandeep Singhal, Frank Claessens, Steven Joniau, Thomas Van den Broeck, Samantha Larkin, Paul A. Townsend, Claire Aukim-Hastie, Manuela Gago-Dominguez, Jose Esteban Castelao, Maria Elena Martinez, Monique J. Roobol, Guido Jenster, Ron H. N. van Schaik, Florence Menegaux, Thérèse Truong, Yves Akoli Koudou, Jianfeng Xu, Kay-Tee Khaw, Lisa Cannon-Albright, Hardev Pandha, Agnieszka Michael, Andrzej Kierzek, Stephen N. Thibodeau, Shannon K. McDonnell, Daniel J. Schaid, Sara Lindstrom, Constance Turman, Jing Ma, David J. Hunter, Elio Riboli, Afshan Siddiq, Federico Canzian, Laurence N. Kolonel, Loic Le Marchand, Robert N. Hoover, Mitchell J. Machiela, Peter Kraft, The PRACTICAL (Prostate Cancer Association Group to Investigate Cancer-Associated Alterations in the Genome) Consortium, Matthew Freedman, Fredrik Wiklund, Stephen Chanock, Brian E. Henderson, Douglas F. Easton, Christopher A. Haiman, Rosalind A. Eeles, David V. Conti, and Zsofia Kote-Jarai
Subjects: Science
Abstract: Prostate cancer (PrCa) involves a large heritable genetic component. Here, the authors perform multivariate fine-mapping of known PrCa GWAS loci, identifying variants enriched for biological function, explaining more familial relative risk, and with potential application in clinical risk profiling.
Published: 2018
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10. Evidence of gene-environment interactions between common breast cancer susceptibility loci and established environmental risk factors.

Author: Stefan Nickels, Thérèse Truong, Rebecca Hein, Kristen Stevens, Katharina Buck, Sabine Behrens, Ursula Eilber, Martina Schmidt, Lothar Häberle, Alina Vrieling, Mia Gaudet, Jonine Figueroa, Nils Schoof, Amanda B Spurdle, Anja Rudolph, Peter A Fasching, John L Hopper, Enes Makalic, Daniel F Schmidt, Melissa C Southey, Matthias W Beckmann, Arif B Ekici, Olivia Fletcher, Lorna Gibson, Isabel dos Santos Silva, Julian Peto, Manjeet K Humphreys, Jean Wang, Emilie Cordina-Duverger, Florence Menegaux, Børge G Nordestgaard, Stig E Bojesen, Charlotte Lanng, Hoda Anton-Culver, Argyrios Ziogas, Leslie Bernstein, Christina A Clarke, Hermann Brenner, Heiko Müller, Volker Arndt, Christa Stegmaier, Hiltrud Brauch, Thomas Brüning, Volker Harth, Genica Network, Arto Mannermaa, Vesa Kataja, Veli-Matti Kosma, Jaana M Hartikainen, kConFab, AOCS Management Group, Diether Lambrechts, Dominiek Smeets, Patrick Neven, Robert Paridaens, Dieter Flesch-Janys, Nadia Obi, Shan Wang-Gohrke, Fergus J Couch, Janet E Olson, Celine M Vachon, Graham G Giles, Gianluca Severi, Laura Baglietto, Kenneth Offit, Esther M John, Alexander Miron, Irene L Andrulis, Julia A Knight, Gord Glendon, Anna Marie Mulligan, Stephen J Chanock, Jolanta Lissowska, Jianjun Liu, Angela Cox, Helen Cramp, Dan Connley, Sabapathy Balasubramanian, Alison M Dunning, Mitul Shah, Amy Trentham-Dietz, Polly Newcomb, Linda Titus, Kathleen Egan, Elizabeth K Cahoon, Preetha Rajaraman, Alice J Sigurdson, Michele M Doody, Pascal Guénel, Paul D P Pharoah, Marjanka K Schmidt, Per Hall, Doug F Easton, Montserrat Garcia-Closas, Roger L Milne, and Jenny Chang-Claude
Subjects: Genetics, QH426-470
Abstract: Various common genetic susceptibility loci have been identified for breast cancer; however, it is unclear how they combine with lifestyle/environmental risk factors to influence risk. We undertook an international collaborative study to assess gene-environment interaction for risk of breast cancer. Data from 24 studies of the Breast Cancer Association Consortium were pooled. Using up to 34,793 invasive breast cancers and 41,099 controls, we examined whether the relative risks associated with 23 single nucleotide polymorphisms were modified by 10 established environmental risk factors (age at menarche, parity, breastfeeding, body mass index, height, oral contraceptive use, menopausal hormone therapy use, alcohol consumption, cigarette smoking, physical activity) in women of European ancestry. We used logistic regression models stratified by study and adjusted for age and performed likelihood ratio tests to assess gene-environment interactions. All statistical tests were two-sided. We replicated previously reported potential interactions between LSP1-rs3817198 and parity (Pinteraction = 2.4 × 10(-6)) and between CASP8-rs17468277 and alcohol consumption (Pinteraction = 3.1 × 10(-4)). Overall, the per-allele odds ratio (95% confidence interval) for LSP1-rs3817198 was 1.08 (1.01-1.16) in nulliparous women and ranged from 1.03 (0.96-1.10) in parous women with one birth to 1.26 (1.16-1.37) in women with at least four births. For CASP8-rs17468277, the per-allele OR was 0.91 (0.85-0.98) in those with an alcohol intake of
Published: 2013
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11. Comparison of 6q25 breast cancer hits from Asian and European Genome Wide Association Studies in the Breast Cancer Association Consortium (BCAC).

Author: Rebecca Hein, Melanie Maranian, John L Hopper, Miroslaw K Kapuscinski, Melissa C Southey, Daniel J Park, Marjanka K Schmidt, Annegien Broeks, Frans B L Hogervorst, H Bas Bueno-de-Mesquita, Kenneth R Muir, Artitaya Lophatananon, Suthee Rattanamongkongul, Puttisak Puttawibul, Peter A Fasching, Alexander Hein, Arif B Ekici, Matthias W Beckmann, Olivia Fletcher, Nichola Johnson, Isabel dos Santos Silva, Julian Peto, Elinor Sawyer, Ian Tomlinson, Michael Kerin, Nicola Miller, Frederick Marmee, Andreas Schneeweiss, Christof Sohn, Barbara Burwinkel, Pascal Guénel, Emilie Cordina-Duverger, Florence Menegaux, Thérèse Truong, Stig E Bojesen, Børge G Nordestgaard, Henrik Flyger, Roger L Milne, Jose Ignacio Arias Perez, M Pilar Zamora, Javier Benítez, Hoda Anton-Culver, Argyrios Ziogas, Leslie Bernstein, Christina A Clarke, Hermann Brenner, Heiko Müller, Volker Arndt, Christa Stegmaier, Nazneen Rahman, Sheila Seal, Clare Turnbull, Anthony Renwick, Alfons Meindl, Sarah Schott, Claus R Bartram, Rita K Schmutzler, Hiltrud Brauch, Ute Hamann, Yon-Dschun Ko, GENICA Network, Shan Wang-Gohrke, Thilo Dörk, Peter Schürmann, Johann H Karstens, Peter Hillemanns, Heli Nevanlinna, Tuomas Heikkinen, Kristiina Aittomäki, Carl Blomqvist, Natalia V Bogdanova, Iosif V Zalutsky, Natalia N Antonenkova, Marina Bermisheva, Darya Prokovieva, Albina Farahtdinova, Elza Khusnutdinova, Annika Lindblom, Sara Margolin, Arto Mannermaa, Vesa Kataja, Veli-Matti Kosma, Jaana Hartikainen, Xiaoqing Chen, Jonathan Beesley, Kconfab Investigators, AOCS Group, Diether Lambrechts, Hui Zhao, Patrick Neven, Hans Wildiers, Stefan Nickels, Dieter Flesch-Janys, Paolo Radice, Paolo Peterlongo, Siranoush Manoukian, Monica Barile, Fergus J Couch, Janet E Olson, Xianshu Wang, Zachary Fredericksen, Graham G Giles, Laura Baglietto, Catriona A McLean, Gianluca Severi, Kenneth Offit, Mark Robson, Mia M Gaudet, Joseph Vijai, Grethe Grenaker Alnæs, Vessela Kristensen, Anne-Lise Børresen-Dale, Esther M John, Alexander Miron, Robert Winqvist, Katri Pylkäs, Arja Jukkola-Vuorinen, Mervi Grip, Irene L Andrulis, Julia A Knight, Gord Glendon, Anna Marie Mulligan, Jonine D Figueroa, Montserrat García-Closas, Jolanta Lissowska, Mark E Sherman, Maartje Hooning, John W M Martens, Caroline Seynaeve, Margriet Collée, Per Hall, Keith Humpreys, Kamila Czene, Jianjun Liu, Angela Cox, Ian W Brock, Simon S Cross, Malcolm W R Reed, Shahana Ahmed, Maya Ghoussaini, Paul D P Pharoah, Daehee Kang, Keun-Young Yoo, Dong-Young Noh, Anna Jakubowska, Katarzyna Jaworska, Katarzyna Durda, Elżbieta Złowocka, Suleeporn Sangrajrang, Valerie Gaborieau, Paul Brennan, James McKay, Chen-Yang Shen, Jyh-Cherng Yu, Huan-Ming Hsu, Ming-Feng Hou, Nick Orr, Minouk Schoemaker, Alan Ashworth, Anthony Swerdlow, Amy Trentham-Dietz, Polly A Newcomb, Linda Titus, Kathleen M Egan, Georgia Chenevix-Trench, Antonis C Antoniou, Manjeet K Humphreys, Jonathan Morrison, Jenny Chang-Claude, Douglas F Easton, and Alison M Dunning
Subjects: Medicine, Science
Abstract: The 6q25.1 locus was first identified via a genome-wide association study (GWAS) in Chinese women and marked by single nucleotide polymorphism (SNP) rs2046210, approximately 180 Kb upstream of ESR1. There have been conflicting reports about the association of this locus with breast cancer in Europeans, and a GWAS in Europeans identified a different SNP, tagged here by rs12662670. We examined the associations of both SNPs in up to 61,689 cases and 58,822 controls from forty-four studies collaborating in the Breast Cancer Association Consortium, of which four studies were of Asian and 39 of European descent. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Case-only analyses were used to compare SNP effects in Estrogen Receptor positive (ER+) versus negative (ER-) tumours. Models including both SNPs were fitted to investigate whether the SNP effects were independent. Both SNPs are significantly associated with breast cancer risk in both ethnic groups. Per-allele ORs are higher in Asian than in European studies [rs2046210: OR (A/G) = 1.36 (95% CI 1.26-1.48), p = 7.6 × 10(-14) in Asians and 1.09 (95% CI 1.07-1.11), p = 6.8 × 10(-18) in Europeans. rs12662670: OR (G/T) = 1.29 (95% CI 1.19-1.41), p = 1.2 × 10(-9) in Asians and 1.12 (95% CI 1.08-1.17), p = 3.8 × 10(-9) in Europeans]. SNP rs2046210 is associated with a significantly greater risk of ER- than ER+ tumours in Europeans [OR (ER-) = 1.20 (95% CI 1.15-1.25), p = 1.8 × 10(-17) versus OR (ER+) = 1.07 (95% CI 1.04-1.1), p = 1.3 × 10(-7), p(heterogeneity) = 5.1 × 10(-6)]. In these Asian studies, by contrast, there is no clear evidence of a differential association by tumour receptor status. Each SNP is associated with risk after adjustment for the other SNP. These results suggest the presence of two variants at 6q25.1 each independently associated with breast cancer risk in Asians and in Europeans. Of these two, the one tagged by rs2046210 is associated with a greater risk of ER- tumours.
Published: 2012
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12. Correction: Comparison of 6q25 Breast Cancer Hits from Asian and European Genome Wide Association Studies in the Breast Cancer Association Consortium (BCAC).

Author: Rebecca Hein, Melanie Maranian, John L. Hopper, Miroslaw K. Kapuscinski, Melissa C. Southey, Daniel J. Park, Marjanka K. Schmidt, Annegien Broeks, Frans B. L. Hogervorst, H. Bas Bueno-de-Mesquit, Kenneth R. Muir, Artitaya Lophatananon, Suthee Rattanamongkongul, Puttisak Puttawibul, Peter A. Fasching, Alexander Hein, Arif B. Ekici, Matthias W. Beckmann, Olivia Fletcher, Nichola Johnson, Isabel dos Santos Silva, Julian Peto, Elinor Sawyer, Ian Tomlinson, Michael Kerin, Nicola Miller, Frederick Marmee, Andreas Schneeweiss, Christof Sohn, Barbara Burwinkel, Pascal Guénel, Emilie Cordina-Duverger, Florence Menegaux, Thérèse Truong, Stig E. Bojesen, Børge G. Nordestgaard, Henrik Flyger, Roger L. Milne, Jose Ignacio Arias Perez, M. Pilar Zamora, Javier Benítez, Hoda Anton-Culver, Argyrios Ziogas, Leslie Bernstein, Christina A. Clarke, Hermann Brenner, Heiko Müller, Volker Arndt, Christa Stegmaier, Nazneen Rahman, Sheila Seal, Clare Turnbull, Anthony Renwick, Alfons Meindl, Sarah Schott, Claus R. Bartram, Rita K. Schmutzler, Hiltrud Brauch, Ute Hamann, Yon-Dschun Ko, Shan Wang-Gohrke, Thilo Dörk, Peter Schürmann, Johann H. Karstens, Peter Hillemanns, Heli Nevanlinna, Tuomas Heikkinen, Kristiina Aittomäki, Carl Blomqvist, Natalia V. Bogdanova, Iosif V. Zalutsky, Natalia N. Antonenkova, Marina Bermisheva, Darya Prokovieva, Albina Farahtdinova, Elza Khusnutdinova, Annika Lindblom, Sara Margolin, Arto Mannermaa, Vesa Kataja, Veli-Matti Kosma, Jaana Hartikainen, Xiaoqing Chen, Jonathan Beesley, kConFab Investigators, Diether Lambrechts, Hui Zhao, Patrick Neven, Hans Wildiers, Stefan Nickels, Dieter Flesch-Janys, Paolo Radice, Paolo Peterlongo, Siranoush Manoukian, Monica Barile, Fergus J. Couch, Janet E. Olson, Xianshu Wang, Zachary Fredericksen, Graham G. Giles, Laura Baglietto, Catriona A. McLean, Gianluca Severi, Kenneth Offit, Mark Robson, Mia M. Gaudet, Joseph Vijai, Grethe Grenaker Alnæs, Vessela Kristensen, Anne-Lise Børresen-Dale, Esther M. John, Alexander Miron, Robert Winqvist, Katri Pylkäs, Arja Jukkola-Vuorinen, Mervi Grip, Irene L. Andrulis, Julia A. Knight, Gord Glendon, Anna Marie Mulligan, Jonine D. Figueroa, Montserrat García-Closas, Jolanta Lissowska, Mark E. Sherman, Maartje Hooning, John W. M. Martens, Caroline Seynaeve, Margriet Collée, Per Hall, Keith Humpreys, Kamila Czene, Jianjun Liu, Angela Cox, Ian W. Brock, Simon S. Cross, Malcolm W. R. Reed, Shahana Ahmed, Maya Ghoussaini, Paul DP. Pharoah, Daehee Kang, Keun-Young Yoo, Dong-Young Noh, Anna Jakubowska, Katarzyna Jaworska, Katarzyna Durda, Elżbieta Złowocka, Suleeporn Sangrajrang, Valerie Gaborieau, Paul Brennan, James McKay, Chen-Yang Shen, Jyh-Cherng Yu, Huan-Ming Hsu, Ming-Feng Hou, Nick Orr, Minouk Schoemaker, Alan Ashworth, Anthony Swerdlow, Amy Trentham-Dietz, Polly A. Newcomb, Linda Titus, Kathleen M. Egan, Georgia Chenevix-Trench, Antonis C. Antoniou, Manjeet K. Humphreys, Jonathan Morrison, Jenny Chang-Claude, Douglas F. Easton, and Alison M. Dunning
Subjects: Medicine, Science
Published: 2012
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13. Sleep Patterns and Risk of Prostate Cancer: A Population-Based Case Control Study in France (EPICAP)

Author: Emilie Cordina-Duverger, Sylvie Cénée, Brigitte Trétarre, Xavier Rebillard, Pierre-Jean Lamy, Gaelle Wendeu-Foyet, and Florence Menegaux
Subjects: Male, Oncology, Risk Factors, Epidemiology, Case-Control Studies, Anti-Inflammatory Agents, Non-Steroidal, Humans, Prostatic Neoplasms, Sleep Deprivation, France, Sleep
Abstract: Background: Sleep disturbances have been singled out for their implication in the risk of several cancer sites. However, results for prostate cancer are still inconsistent. Methods: We used data from the EPICAP study, a French population-based case–control study including 819 incident prostate cancer cases and 879 controls frequency matched by age. Detailed information on sleep duration on work/free days, and sleep medication over lifetime was collected. Results: Sleep duration and sleep deprivation were not associated with prostate cancer, whatever the aggressiveness of prostate cancer. However, sleep deprivation was associated with an increased prostate cancer risk among men with an evening chronotype [OR, 1.96; 95% confidence interval (CI), 1.04–3.70]. We also observed an increased risk of prostate cancer with higher duration of sleep medication use (Ptrend = 0.008). This association with long duration of sleep medication use (≥10 years) was more pronounced among men who worked at night 15 years or more (OR, 3.84; 95% CI, 1.30–11.4) and among nonusers of NSAID (OR, 2.08; 95% CI, 1.15–3.75). Conclusions: Our results suggested that chronotype, night work, or NSAID use could modify the association between sleep disorders and prostate cancer occurrence needing further investigations to go further. Impact: EPICAP is the first study, which investigates several sleep indicators taking into account potential effect modifiers. If our findings were confirmed, we could identify subgroups of men at higher risk of prostate cancer that may be accessible to preventive measures.
Published: 2022
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14. Sexually and non-sexually transmitted infections and the risk of Prostate Cancer: results from the EPICAP study

Author: Melissa Sawaya, Emilie Cordivadverger, Pierre-Jean Lamy, Xavier Rebillard, Brigitte Tretarre, and Florence Menegaux
Subjects: Health (social science), Epidemiology, Health Policy, Public Health, Environmental and Occupational Health, Medicine (miscellaneous), Health Informatics
Published: 2023
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15. Supplementary Tables 1-13 from 19p13.1 Is a Triple-Negative–Specific Breast Cancer Susceptibility Locus

Author: Fergus J. Couch, Douglas F. Easton, Ylermi Soini, Jaana M. Hartikainen, Veli-Matti Kosma, Arto Mannermaa, Xiaoqing Chen, Jonathan Beesley, Georgia Chenevix-Trench, Marie-Rose Christiaens, Anne-Sophie Dieudonne, Sigrid Hatse, Diether Lambrechts, Monica Barile, Siranoush Manoukian, Paolo Peterlongo, Paolo Radice, Janet E. Olson, Susan Slager, V.S. Pankratz, Matthew L. Kosel, Gianluca Severi, Catriona A. McLean, Laura Baglietto, Graham G. Giles, Anne-Lise Børresen-Dale, Vessela Kristensen, Grethe Grenaker Alnæs, Alexander Miron, Esther M. John, Mervi Grip, Arja Jukkola-Vuorinen, Katri Pylkäs, Robert Winqvist, Anna Marie Mulligan, Gord Glendon, Julia A. Knight, Irene L. Andrulis, Maartje J. Hooning, Rob A.E.M. Tollenaar, Caroline Seynaeve, Peter Devilee, Jolanta Lissowska, Mark E. Sherman, Jonine D. Figueroa, Montserrat Garcia-Closas, Diana M. Eccles, Helena Hwang, Foluso Ademuyiwa, Christine B. Ambrosone, Kamila Czene, Per Hall, Malcom W. Reed, Simon S. Cross, Angela Cox, Qin Wang, Manjeet K. Humphreys, Alison M. Dunning, Paul P. Pharoah, Hans Ulrich Ulmer, Thomas Rüdiger, Thomas Dünnebier, Ute Hamann, Chia-Ni Hsiung, Huan-Ming Hsu, Jyh-Cherng Yu, Chen-Yang Shen, Christina Clarke Dur, Leslie Bernstein, Argyrios Ziogas, Hoda Anton-Culver, Minouk J. Schoemaker, Nicholas Orr, Alan Ashworth, Anthony J. Swerdlow, Melissa C. Southey, Daniel J. Park, Carmel Apicella, John L. Hopper, Efraim H. Rosenberg, Linde M. Braaf, Annegien Broeks, Marjanka K. Schmidt, Surapon Wiangnon, Puttisak Puttawibul, Kenneth Muir, Artitaya Lophatananon, Arif B. Ekici, Arndt Hartmann, Matthias W. Beckmann, Peter A. Fasching, Isabel dos Santos Silva, Olivia Fletcher, Nichola Johnson, Julian Peto, Michael J. Kerin, Ian Tomlinson, Elinor Sawyer, Christof Sohn, Andreas Schneeweiss, Frederick Marmé, Barbara Burwinkel, Emilie Cordina-Duverger, Florence Menegaux, Thérèse Truong, Pascal Guénel, Henrik Flyger, Børge G. Nordestgaard, Sune F. Nielsen, Stig E. Bojesen, José Ignacio Arias Pérez, María Pilar Zamora, Javier Benítez, Roger L. Milne, Annie Perkins, Miriam Dwek, Ruth Swann, Helen J. Gogas, George Fountzilas, Alexandra Stavropoulou, Drakoulis Yannoukakos, Penelope Miron, Christa Stegmaier, Volker Arndt, Heiko Müller, Hermann Brenner, Priyanka Sharma, Harsh B. Pathak, JoEllen Weaver, Andrew K. Godwin, Christoph Engel, Sarah Schott, Claus R. Bartram, Alfons Meindl, Rita K. Schmutzler, Hans-Peter Fischer, Yon-Dschun Ko, Hiltrud Brauch, Stefan Nickels, Shan Wang-Gohrke, Hans-Peter Sinn, Dieter Flesch-Janys, Alina Vrieling, Jenny Chang-Claude, Carl Blomqvist, Kristiina Aittomäki, Dario Greco, Heli Nevanlinna, Annika Lindblom, Sara Margolin, Xianshu Wang, Celine M. Vachon, Zachary Fredericksen, and Kristen N. Stevens
Abstract: PDF file - 272K
Published: 2023
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16. Evidence of Novel Susceptibility Variants for Prostate Cancer and a Multiancestry Polygenic Risk Score Associated with Aggressive Disease in Men of African Ancestry

Author: Fei Chen, Ravi K. Madduri, Alex A. Rodriguez, Burcu F. Darst, Alisha Chou, Xin Sheng, Anqi Wang, Jiayi Shen, Edward J. Saunders, Suhn K. Rhie, Jeannette T. Bensen, Sue A. Ingles, Rick A. Kittles, Sara S. Strom, Benjamin A. Rybicki, Barbara Nemesure, William B. Isaacs, Janet L. Stanford, Wei Zheng, Maureen Sanderson, Esther M. John, Jong Y. Park, Jianfeng Xu, Ying Wang, Sonja I. Berndt, Chad D. Huff, Edward D. Yeboah, Yao Tettey, Joseph Lachance, Wei Tang, Christopher T. Rentsch, Kelly Cho, Benjamin H. Mcmahon, Richard B. Biritwum, Andrew A. Adjei, Evelyn Tay, Ann Truelove, Shelley Niwa, Thomas A. Sellers, Kosj Yamoah, Adam B. Murphy, Dana C. Crawford, Alpa V. Patel, William S. Bush, Melinda C. Aldrich, Olivier Cussenot, Gyorgy Petrovics, Jennifer Cullen, Christine M. Neslund-Dudas, Mariana C. Stern, Zsofia Kote-Jarai, Koveela Govindasami, Michael B. Cook, Anand P. Chokkalingam, Ann W. Hsing, Phyllis J. Goodman, Thomas J. Hoffmann, Bettina F. Drake, Jennifer J. Hu, Jacob M. Keaton, Jacklyn N. Hellwege, Peter E. Clark, Mohamed Jalloh, Serigne M. Gueye, Lamine Niang, Olufemi Ogunbiyi, Michael O. Idowu, Olufemi Popoola, Akindele O. Adebiyi, Oseremen I. Aisuodionoe-Shadrach, Hafees O. Ajibola, Mustapha A. Jamda, Olabode P. Oluwole, Maxwell Nwegbu, Ben Adusei, Sunny Mante, Afua Darkwa-Abrahams, James E. Mensah, Halimatou Diop, Stephen K. Van Den Eeden, Pascal Blanchet, Jay H. Fowke, Graham Casey, Anselm J. Hennis, Alexander Lubwama, Ian M. Thompson, Robin Leach, Douglas F. Easton, Michael H. Preuss, Ruth J. Loos, Susan M. Gundell, Peggy Wan, James L. Mohler, Elizabeth T. Fontham, Gary J. Smith, Jack A. Taylor, Shiv Srivastava, Rosaline A. Eeles, John D. Carpten, Adam S. Kibel, Luc Multigner, Marie-Élise Parent, Florence Menegaux, Geraldine Cancel-Tassin, Eric A. Klein, Caroline Andrews, Timothy R. Rebbeck, Laurent Brureau, Stefan Ambs, Todd L. Edwards, Stephen Watya, Stephen J. Chanock, John S. Witte, William J. Blot, J. Michael Gaziano, Amy C. Justice, David V. Conti, Christopher A. Haiman, University of Southern California (USC), Keck School of Medicine [Los Angeles], Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], Centre de recherche en épidémiologie et santé des populations (CESP), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay
Subjects: Prostate cancer, MESH: Humans, Urology, MESH: Genetic Predisposition to Disease, MESH: Black People, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Male, Polygenic risk score, African ancestry, MESH: Risk Factors, MESH: Prostatic Neoplasms, MESH: Genome-Wide Association Study, Susceptibility loci, Aggressive prostate cancer
Abstract: Background: Genetic factors play an important role in prostate cancer (PCa) susceptibility.Objective: To discover common genetic variants contributing to the risk of PCa in men of African ancestry.Design, setting, and participants: We conducted a meta-analysis of ten genome-wide association studies consisting of 19378 cases and 61620 controls of African ancestry.Outcome measurements and statistical analysis: Common genotyped and imputed variants were tested for their association with PCa risk. Novel susceptibility loci were identified and incorporated into a multiancestry polygenic risk score (PRS). The PRS was evaluated for associations with PCa risk and disease aggressiveness.Results and limitations: Nine novel susceptibility loci for PCa were identified, of which seven were only found or substantially more common in men of African ancestry, including an African-specific stop-gain variant in the prostate-specific gene anoctamin 7 (ANO7). A multiancestry PRS of 278 risk variants conferred strong associations with PCa risk in African ancestry studies (odds ratios [ORs] >3 and >5 for men in the top PRS decile and percentile, respectively). More importantly, compared with men in the 40-60% PRS category, men in the top PRS decile had a significantly higher risk of aggressive PCa (OR = 1.23, 95% confidence interval = 1.10-1.38, p = 4.4 × 10-4).Conclusions: This study demonstrates the importance of large-scale genetic studies in men of African ancestry for a better understanding of PCa susceptibility in this high-risk population and suggests a potential clinical utility of PRS in differentiating between the risks of developing aggressive and nonaggressive disease in men of African ancestry.Patient summary: In this large genetic study in men of African ancestry, we discovered nine novel prostate cancer (PCa) risk variants. We also showed that a multiancestry polygenic risk score was effective in stratifying PCa risk, and was able to differentiate risk of aggressive and nonaggressive disease.
Published: 2023
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17. Marital status and prostate cancer incidence: a pooled analysis of 12 case–control studies from the PRACTICAL consortium

Author: C. Slavov, Radka Kaneva, Geraldine Cancel-Tassin, Azad Hassan Abdul Razack, Rosalind A. Eeles, Jong Y. Park, Nora Pashayan, Elaine A. Ostrander, Lixin Song, Manuela Gago-Dominguez, Charlotte Salmon, Olivier Cussenot, Apcb BioResource, Manolis Kogevinas, Jasmine Lim, Emilie Cordina-Duverger, Florence Menegaux, Jyotsna Batra, Javier Llorca, Suzanne K Chambers, Hui-Yi Lin, Jose E. Castelao, Zsofia Kote-Jarai, Janet L. Stanford, Marie-Élise Parent, Alison M. Dunning, and Kenneth Muir
Subjects: medicine.medical_specialty, Epidemiology, business.industry, Incidence (epidemiology), Case-control study, Cancer, consortium, Odds ratio, prostate cancer, medicine.disease, 3. Good health, meta-analysis, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, 030220 oncology & carcinogenesis, Meta-analysis, Marital status, Medicine, 030212 general & internal medicine, pooled analysis, business, marital status, Demography
Abstract: While being in a committed relationship is associated with a better prostate cancer prognosis, little is known about how marital status relates to its incidence. Social support provided by marriage/relationship could promote a healthy lifestyle and an increased healthcare seeking behavior. We investigated the association between marital status and prostate cancer risk using data from the PRACTICAL Consortium. Pooled analyses were conducted combining 12 case–control studies based on histologically-confirmed incident prostate cancers and controls with information on marital status prior to diagnosis/interview. Marital status was categorized as married/partner, separated/divorced, single, or widowed. Tumours with Gleason scores ≥ 8 defined high-grade cancers, and low-grade otherwise. NCI-SEER’s summary stages (local, regional, distant) indicated the extent of the cancer. Logistic regression was used to derive odds ratios (ORs) and 95% confidence intervals (CI) for the association between marital status and prostate cancer risk, adjusting for potential confounders. Overall, 14,760 cases and 12,019 controls contributed to analyses. Compared to men who were married/with a partner, widowed men had an OR of 1.19 (95% CI 1.03–1.35) of prostate cancer, with little difference between low- and high-grade tumours. Risk estimates among widowers were 1.14 (95% CI 0.97–1.34) for local, 1.53 (95% CI 1.22–1.92) for regional, and 1.56 (95% CI 1.05–2.32) for distant stage tumours. Single men had elevated risks of high-grade cancers. Our findings highlight elevated risks of incident prostate cancer among widowers, more often characterized by tumours that had spread beyond the prostate at the time of diagnosis. Social support interventions and closer medical follow-up in this sub-population are warranted.
Published: 2021
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18. Occupational heat exposure and prostate cancer risk: A pooled analysis of case-control studies

Author: Alice Hinchliffe, Juan Alguacil, Wendy Bijoux, Manolis Kogevinas, Florence Menegaux, Marie-Elise Parent, Beatriz Pérez Gomez, Sanni Uuksulainen, and Michelle C. Turner
Subjects: Male, Prostate cancer, Hot Temperature, Prostatic Neoplasms, Case-control study, Biochemistry, Heat stress, Pooled analysis, Occupational Diseases, Logistic Models, 32 Ciencias Médicas, Risk Factors, Occupational heat exposure, Case-Control Studies, Occupational Exposure, General Earth and Planetary Sciences, Humans, General Environmental Science
Abstract: Background: Heat exposures occur in many occupations. Heat has been linked to key carcinogenic processes, however, evidence for associations with cancer risk is sparse. We examined potential associations between occupational heat exposure and prostate cancer risk in a multi-country study. Methods: We analysed a large, pooled dataset of 3142 histologically confirmed prostate cancer cases and 3512 frequency-matched controls from three countries: Canada, France, and Spain. Three exposure indices: ever exposure, lifetime cumulative exposure and duration of exposure, were developed using the Finnish Job- Exposure Matrix, FINJEM, applied to the lifetime occupational history of participants. We estimated odds ratios (ORs) and 95% confidence intervals (CIs), using conditional logistic regression models stratified by 5-year age groups and study, adjusting for potential confounders. Potential interactions with exposure to other occupational agents were also explored. Results: Overall, we found no association for ever occupational heat exposure (OR 0.97; 95% CI 0.87, 1.09), nor in the highest categories of lifetime cumulative exposure (OR 1.04; 95% CI 0.89, 1.23) or duration (OR 1.03; 95% CI 0.88, 1.22). When using only the Spanish case-control study and a Spanish Job Exposure Matrix (JEM), some weakly elevated ORs were observed. Conclusions: Findings from this study provide no clear evidence for an association between occupational heat exposure and prostate cancer risk., The study was partially funded by the "Accion Transversal del Cancer", approved by the Spanish Ministry Council on October 11, 2007, by the Instituto de Salud Carlos III-FEDER (PI08/1770, PI08/1359, PI09/00773, PI09/01286, PI09/01903, PI09/02078, PI09/01662, PI11/01403, PI11/01889, PI12/00265), the Fundación Marqués de Valdecilla (API 10/09), the Junta de Castilla y León (LE22A10–2), the Consejería de Salud of the Junta de Andalucía (2009-S0143), the Conselleria de Sanitat of the Generalitat Valenciana (AP_061/10), the Recercaixa (2010ACUP 00310), the Regional Government of the Basque Country, the Consejería de Sanidad de la Región de Murcia, the European Commission grants FOOD-CT-2006–036224-HIWATE, the Spanish Association Against Cancer (AECC) Scientific Foundation, the Catalan Government DURSI grant 2014SGR647, the Fundación Caja de Ahorros de Asturias and by the University of Oviedo. MCT is funded by a Ramón y Cajal fellowship (RYC-2017-01892) from the Spanish Ministry of Science, Innovation and Universities and co-funded by the European Social Fund. We acknowledge support from the Spanish Ministry of Science and Innovation through the “Centro de Excelencia Severo Ochoa 2019–2023” Program (CEX 2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program. PROtEuS was supported financially through grants from the Canadian Cancer Society (grants no. 13149, 19,500, 19,864 and 19,865), the Cancer Research Society, the Fonds de Recherche du Québec-Santé (FRQS), FRQSR Réseau de recherche en santé environnementale, the Ministère du Développement économique, de l’Innovation et de l’Exportation du Québec, and the Canadian Institutes of Health Research (grant no. 159704). The EPICAP Study was funded by Ligue nationale contre le cancer, Ligue contre le cancer du Val-de-Marne, Fondation de France, Agence nationale de securite sanitaire de l’alimentation, de l’environnement et du travail (ANSES).
Published: 2022

19. Adiposity and Endometrial Cancer Risk in Postmenopausal Women: A Sequential Causal Mediation Analysis

Author: Sofia Christakoudi, Christina C. Dahm, Rudolf Kaaks, Vivian Viallon, Renée T. Fortner, J. Ramón Quirós, Margarita Moreno-Betancur, Gianluca Severi, Florence Menegaux, Eva Ardanaz, Antonio Agudo, Julie A. Simpson, María José Sánchez, Jytte Halkjær, Marc J. Gunter, Naomi E. Allen, Amalia Karahalios, Sabina Rinaldi, S. Ghazaleh Dashti, Sandra Colorado-Yohar, Carine Biessy, Matthias B. Schulze, Konstantinos K. Tsilidis, Alessandra Macciotta, Dallas R. English, Elio Riboli, Vittorio Perduca, Sabina Sieri, Giovanna Masala, Anne M. May, Rosario Tumino, Anne Tjønneland, Laure Dossus, Salvatore Panico, Pilar Amiano, Elisabete Weiderpass, Anouk E. Hiensch, Krasimira Aleksandrova, Pietro Ferrari, and Helene Tilma Vistisen
Subjects: 0301 basic medicine, Oncology, medicine.medical_specialty, Epidemiology, medicine.drug_class, Estrone, Body Mass Index, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, Internal medicine, Odds Ratio, medicine, Hyperinsulinemia, Humans, Obesity, Prospective Studies, 11 Medical and Health Sciences, Adiposity, C-Peptide, Adiponectin, business.industry, Endometrial cancer, Cancer, Estrogens, medicine.disease, Endometrial Neoplasms, European Prospective Investigation into Cancer and Nutrition, Causality, Postmenopause, 030104 developmental biology, chemistry, Estrogen, Case-Control Studies, 030220 oncology & carcinogenesis, Female, business, Body mass index, Biomarkers
Abstract: Background: Adiposity increases endometrial cancer risk, possibly through inflammation, hyperinsulinemia, and increasing estrogens. We aimed to quantify the mediating effects of adiponectin (anti-inflammatory adipocytokine); IL6, IL1-receptor antagonist, TNF receptor 1 and 2, and C-reactive protein (inflammatory status biomarkers); C-peptide (hyperinsulinemia biomarker); and free estradiol and estrone (estrogen biomarkers) in the adiposity–endometrial cancer link in postmenopausal women. Methods: We used data from a case–control study within the European Prospective Investigation into Cancer and Nutrition (EPIC). Eligible women did not have cancer, hysterectomy, and diabetes; did not use oral contraceptives or hormone therapy; and were postmenopausal at recruitment. Mediating pathways from adiposity to endometrial cancer were investigated by estimating natural indirect (NIE) and direct (NDE) effects using sequential mediation analysis. Results: The study included 163 cases and 306 controls. The adjusted OR for endometrial cancer for body mass index (BMI) ≥30 versus ≥18.5− Conclusions: Reduced adiponectin and increased inflammatory biomarkers, C-peptide, and estrogens mediated approximately 70% of increased odds of endometrial cancer in women with obesity versus normal weight. Impact: If replicated, these results could have implications for identifying targets for intervention to reduce endometrial cancer risk in women with obesity.
Published: 2021
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20. Prostate cancer risk stratification improvement across multiple ancestries with new polygenic hazard score

Author: Minh-Phuong, Huynh-Le, Roshan, Karunamuni, Chun Chieh, Fan, Lui, Asona, Wesley K, Thompson, Maria Elena, Martinez, Rosalind A, Eeles, Zsofia, Kote-Jarai, Kenneth R, Muir, Artitaya, Lophatananon, Johanna, Schleutker, Nora, Pashayan, Jyotsna, Batra, Henrik, Grönberg, David E, Neal, Børge G, Nordestgaard, Catherine M, Tangen, Robert J, MacInnis, Alicja, Wolk, Demetrius, Albanes, Christopher A, Haiman, Ruth C, Travis, William J, Blot, Janet L, Stanford, Lorelei A, Mucci, Catharine M L, West, Sune F, Nielsen, Adam S, Kibel, Olivier, Cussenot, Sonja I, Berndt, Stella, Koutros, Karina Dalsgaard, Sørensen, Cezary, Cybulski, Eli Marie, Grindedal, Florence, Menegaux, Jong Y, Park, Sue A, Ingles, Christiane, Maier, Robert J, Hamilton, Barry S, Rosenstein, Yong-Jie, Lu, Stephen, Watya, Ana, Vega, Manolis, Kogevinas, Fredrik, Wiklund, Kathryn L, Penney, Chad D, Huff, Manuel R, Teixeira, Luc, Multigner, Robin J, Leach, Hermann, Brenner, Esther M, John, Radka, Kaneva, Christopher J, Logothetis, Susan L, Neuhausen, Kim, De Ruyck, Piet, Ost, Azad, Razack, Lisa F, Newcomb, Jay H, Fowke, Marija, Gamulin, Aswin, Abraham, Frank, Claessens, Jose Esteban, Castelao, Paul A, Townsend, Dana C, Crawford, Gyorgy, Petrovics, Ron H N, van Schaik, Marie-Élise, Parent, Jennifer J, Hu, Wei, Zheng, Ian G, Mills, Ole A, Andreassen, Anders M, Dale, Tyler M, Seibert, collaborators, UKGPCS, BioResource), APCB (Australian Prostate Cancer, Investigators, NC-LA PCaP, Collaborators, IMPACT Study Steering Committee and, Investigators, Canary PASS, Committee, Profile Study Steering, Consortium, PRACTICAL, and Clinical Chemistry
Subjects: SELECTION, Male, Cancer Research, Urology, LASSO, Polymorphism, Single Nucleotide, Risk Assessment, Cancer screening, Cancer epidemiology, SDG 3 - Good Health and Well-being, Risk Factors, Humans, Genetic Predisposition to Disease, prostate cancer, multi-ancestry datasets, Cancer genetics, Early Detection of Cancer, Prostatic Neoplasms/diagnosis, Cancer och onkologi, Science & Technology, Manchester Cancer Research Centre, ResearchInstitutes_Networks_Beacons/mcrc, Prostatic Neoplasms, Urology & Nephrology, Prostate-Specific Antigen, Prostate-Specific Antigen/genetics, Oncology, Cancer and Oncology, Life Sciences & Biomedicine
Abstract: Background Prostate cancer risk stratification using single-nucleotide polymorphisms (SNPs) demonstrates considerable promise in men of European, Asian, and African genetic ancestries, but there is still need for increased accuracy. We evaluated whether including additional SNPs in a prostate cancer polygenic hazard score (PHS) would improve associations with clinically significant prostate cancer in multi-ancestry datasets. Methods In total, 299 SNPs previously associated with prostate cancer were evaluated for inclusion in a new PHS, using a LASSO-regularized Cox proportional hazards model in a training dataset of 72,181 men from the PRACTICAL Consortium. The PHS model was evaluated in four testing datasets: African ancestry, Asian ancestry, and two of European Ancestry—the Cohort of Swedish Men (COSM) and the ProtecT study. Hazard ratios (HRs) were estimated to compare men with high versus low PHS for association with clinically significant, with any, and with fatal prostate cancer. The impact of genetic risk stratification on the positive predictive value (PPV) of PSA testing for clinically significant prostate cancer was also measured. Results The final model (PHS290) had 290 SNPs with non-zero coefficients. Comparing, for example, the highest and lowest quintiles of PHS290, the hazard ratios (HRs) for clinically significant prostate cancer were 13.73 [95% CI: 12.43–15.16] in ProtecT, 7.07 [6.58–7.60] in African ancestry, 10.31 [9.58–11.11] in Asian ancestry, and 11.18 [10.34–12.09] in COSM. Similar results were seen for association with any and fatal prostate cancer. Without PHS stratification, the PPV of PSA testing for clinically significant prostate cancer in ProtecT was 0.12 (0.11–0.14). For the top 20% and top 5% of PHS290, the PPV of PSA testing was 0.19 (0.15–0.22) and 0.26 (0.19–0.33), respectively. Conclusions We demonstrate better genetic risk stratification for clinically significant prostate cancer than prior versions of PHS in multi-ancestry datasets. This is promising for implementing precision-medicine approaches to prostate cancer screening decisions in diverse populations.
Published: 2022
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21. A Germline Variant at 8q24 Contributes to Familial Clustering of Prostate Cancer in Men of African Ancestry

Author: Luc Multigner, William J. Blot, Alexander Lubwama, Stephen Watya, Peter E. Clark, Lucy Xia, Sara S. Strom, Adam S. Kibel, Jong Y. Park, Adam B. Murphy, Jennifer Cullen, Christopher A. Haiman, Florence Menegaux, Shiv Srivastava, Loreall Pooler, Mariana C. Stern, Anand P. Chokkalingam, Eric A. Klein, Wei Zheng, Thomas A. Sellers, Anselm Hennis, Dana C. Crawford, James L. Mohler, Jack A. Taylor, Esther M. John, Robin J. Leach, Sonja I. Berndt, Laurent Brureau, John D. Carpten, Susan Gundell, David V. Conti, Barbara Nemesure, Rosalind A. Eeles, Graham Casey, Pascal Blanchet, Benjamin A. Rybicki, Chad D. Huff, Maureen Sanderson, Stephen J. Chanock, Melinda C. Aldrich, Jay H. Fowke, Jennifer J. Hu, Diptasri Mandal, Sue A. Ingles, Kosj Yamoah, Kathleen A. Cooney, K. Govindasami, Ian M. Thompson, Patrick C. Walsh, Xin Sheng, Zsofia Kote-Jarai, Janet L. Stanford, Marie-Élise Parent, Christine Neslund-Dudas, Jianfeng Xu, William S. Bush, Phyllis J. Goodman, Meredith Yeager, Burcu F. Darst, Gary J. Smith, Victoria L. Stevens, Rick A. Kittles, Elaine A. Ostrander, Olivier Cussenot, Gyorgy Petrovics, Elizabeth T. H. Fontham, William B. Isaacs, Peggy Wan, Geraldine Cancel-Tassin, Susan M. Gapstur, Bettina F. Drake, Jeannette T. Bensen, University of Southern California (USC), Centre de Recherche pour les Pathologies Prostatiques. (CeRePP / UA 3104), CEREPP, CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], U19 CA148537, U19 CA214253, R01 CA165862, and K99 CA246063, National Cancer Institute at the National Institutes of Health, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)
Subjects: Male, Oncology, medicine.medical_specialty, Urology, Family history, Population, 030232 urology & nephrology, Black People, Familial prostate cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, Familial clustering, Risk Assessment, Article, Germline, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Internal medicine, Genetics, Humans, Medicine, education, Genetic variant, Aged, education.field_of_study, business.industry, Genetic Variation, Prostatic Neoplasms, 8q24, Middle Aged, medicine.disease, Health equity, 3. Good health, Disease Hotspot, Germ Cells, Prostate cancer screening, African ancestry, 030220 oncology & carcinogenesis, Health disparities, business
Abstract: International audience; Although men of African ancestry have a high risk of prostate cancer (PCa), no genes or mutations have been identified that contribute to familial clustering of PCa in this population. We investigated whether the African ancestry-specific PCa risk variant at 8q24, rs72725854, is enriched in men with a PCa family history in 9052 cases, 143 cases from high-risk families, and 8595 controls of African ancestry. We found the risk allele to be significantly associated with earlier age at diagnosis, more aggressive disease, and enriched in men with a PCa family history (32% of high-risk familial cases carried the variant vs 23% of cases without a family history and 12% of controls). For cases with two or more first-degree relatives with PCa who had at least one family member diagnosed at age
Published: 2020
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22. P-220 Assessing prostate cancer risk among protective service workers and health professionals

Author: Manolis Kogevinas, Wendy Bijoux, Hugues Richard, Marie-Élise Parent, Ana Espinosa, and Florence Menegaux
Subjects: education.field_of_study, Health professionals, business.industry, Confounding, Population, Odds ratio, International Standard Classification of Occupations, medicine.disease, Logistic regression, Confidence interval, Prostate cancer, Medicine, business, education, Demography
Abstract: Introduction Fire-fighting occupations and nightshift work are possibly/probably carcinogenic to humans (Groups 2A/2B), according to IARC. Some recent studies also found a higher risk for prostate cancer (PCa) for these occupational categories. However, results are inconsistent and most did not consider the aggressiveness of the tumour. Objectives To study the risk of PCa among protective service workers and medical professionals, occupations frequently entailing night-shift work, with a particular interest for aggressive cancers. Methods EPICAP, PROtEuS and MCC-SPAIN are three population-based case-control studies conducted respectively in France, Canada and Spain that included overall 3,859 PCa cases newly diagnosed between 2005 and 2014 in men ≤ 85 years old and 4,359 population-based controls frequency-matched on age. Participants have been interviewed face-to-face on their socio-demographic characteristics, lifestyle, leisure activities and complete occupational history for each job held. Occupations were coded using the International Standard Classification of Occupations 1988. Unconditional logistic regressions were performed to assess the association between selected occupations and PCa risk, using the Gleason score at diagnosis, after adjusting for potential confounders. Results Regarding protective service occupations, we observed positive associations with PCa among participants who has ever worked as police officers (odds ratio (OR)=1.49 [95% confidence interval 1.03 ; 2.17]), as police inspectors and detectives (OR=1.90 [1.06 ; 3.40]), and as fire-fighters (OR=1.62 [0.92 ; 2.86]). We found a negative association for those who ever worked in the armed forces (OR=0.67 [0.53 ; 0.86]). Positive associations with PCa were observed for health professionals (except nursing) who had worked ≥10 years (OR=1.54 [0.99 ; 2.39]). Analyses taking into account PCa aggressiveness, screening and nightshift work are in progress. Conclusion Excess PCa risks were observed for occupations that involve a high frequency of nightshift work.
Published: 2021
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23. Diabetes, metabolic syndrome and prostate cancer risk: Results from the EPICAP case-control study

Author: Céline Lavalette, Emilie Cordina-Duverger, Xavier Rébillard, Pierre-Jean Lamy, Brigitte Trétarre, Sylvie Cénée, and Florence Menegaux
Subjects: Cancer Research, Oncology, Epidemiology
Abstract: Diabetes may be associated with decreased prostate cancer (PCa) risk. However, previous studies have not always accounted for time since diabetes diagnosis or antidiabetic drug use. Futhermore, the role of metabolic syndrome (MetS) in PCa risk is still debated. We investigated the role of diabetes and MetS in PCa risk based on data from the Epidemiological study of PCa (EPICAP).EPICAP is a population-based case-control study that included 819 incident PCa cases in 2012-2013 and 879 controls frequency matched by age. MetS was characterized according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III). Logistic regression models adjusted for age, family history of PCa and ethnicity, were used to assess odds ratios (ORs) and their 95%conficence intervals (CIs) for the associations between diabetes, MetS and PCa risk.Whereas we did not observed an association between diabetes and PCa, a decreased risk of PCa has been highlighted with an increasing treated diabetes duration (p-trend=0.008). No association has been observed between MetS, the number of MetS criteria and the risk of PCa. However, we suggested that NSAIDs use could modify the association between MetS and PCa risk.Our results suggest an inverse association between the duration of diabetes and PCa risk. The role of metabolic factors, such as MetS and its components, in PCa risk remains unclear and requires further investigations.
Published: 2022
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24. Prostate cancer risk stratification improved across multiple ancestries with new polygenic hazard score

Author: Christopher J. Logothetis, Manolis Kogevinas, Piet Ost, Jong Y. Park, Minh-Phuong Huynh-Le, Johanna Schleutker, Jose E. Castelao, Apcb, Stella Koutros, Canary Pass Investigators, Rosalind A. Eeles, Robin J. Leach, David E. Neal, Janet L. Stanford, Ana Vega, Roshan Karunamuni, Radka Kaneva, Olivier Cussenot, Azad Hassan Abdul Razack, Anders M. Dale, Gyorgy Petrovics, Wei Zheng, Sue A. Ingles, William J. Blot, Esther M. John, Chun Chieh Fan, Ruth C. Travis, Lorelei A. Mucci, Robert J. Hamilton, Wesley K. Thompson, Luc Multigner, Demetrius Albanes, Artitaya Lophatananon, Fredrik Wiklund, Marie-Élise Parent, Christopher A. Haiman, Frank Claessens, Florence Menegaux, Susan L. Neuhausen, Alicja Wolk, Maria Elena Martinez, Kathryn L. Penney, Catherine M. Tangen, Tyler M. Seibert, Jennifer J. Hu, Hermann Brenner, Sune F. Nielsen, Jyotsna Batra, Marija Gamulin, Ian G. Mills, Nc-La PCaP Investigators, Christiane Maier, Barry S. Rosenstein, Stephen Watya, Aswin George Abraham, Manuel R. Teixeira, Lui Asona, Yong-Jie Lu, Kim De Ruyck, Paul A Townsend, Sonja I. Berndt, Eli Marie Grindedal, Ole A. Andreassen, Catharine M L West, Ron H.N. van Schaik, Zsofia Kote-Jarai, Lisa F. Newcomb, Kenneth Muir, Børge G. Nordestgaard, Karina Dalsgaard Sørensen, Chad D. Huff, Jay H. Fowke, Henrik Grönberg, Dana C. Crawford, Adam S. Kibel, Robert J. MacInnis, Cezary Cybulski, and Nora Pashayan
Subjects: Oncology, Prostate cancer risk, medicine.medical_specialty, business.industry, Proportional hazards model, Hazard ratio, Single-nucleotide polymorphism, medicine.disease, Prostate cancer, Prostate cancer screening, Internal medicine, Cohort, medicine, Genetic risk, business
Abstract: IntroductionProstate cancer risk stratification using single-nucleotide polymorphisms (SNPs) demonstrates considerable promise in men of European, Asian, and African genetic ancestries, but there is still need for increased accuracy. We evaluated whether including additional SNPs in a prostate cancer polygenic hazard score (PHS) would improve associations with clinically significant prostate cancer in multi-ancestry datasets.MethodsIn total, 299 SNPs previously associated with prostate cancer were evaluated for inclusion in a new PHS, using a LASSO-regularized Cox proportional hazards model in a training dataset of 72,181 men from the PRACTICAL Consortium. The PHS model was evaluated in four testing datasets: African ancestry, Asian ancestry, and two of European Ancestry—the Cohort of Swedish Men (COSM) and the ProtecT study. Hazard ratios (HRs) were estimated to compare men with high versus low PHS for association with clinically significant, with any, and with fatal prostate cancer. The impact of genetic risk stratification on the positive predictive value (PPV) of PSA testing for clinically significant prostate cancer was also measured.ResultsThe final model (PHS290) had 290 SNPs with non-zero coefficients. Comparing, for example, the highest and lowest quintiles of PHS290, the hazard ratios (HRs) for clinically significant prostate cancer were 13.73 [95% CI: 12.43-15.16] in ProtecT, 7.07 [6.58-7.60] in African ancestry, 10.31 [9.58-11.11] in Asian ancestry, and 11.18 [10.34-12.09] in COSM. Similar results were seen for association with any and fatal prostate cancer. Without PHS stratification, the PPV of PSA testing for clinically significant prostate cancer in ProtecT was 0.12 (0.11-0.14). For the top 20% and top 5% of PHS290, the PPV was 0.19 (0.15-0.22) and 0.26 (0.19-0.33), respectively.ConclusionWe demonstrate better genetic risk stratification for clinically significant prostate cancer than prior versions of PHS in multi-ancestry datasets. This is promising for implementing precision-medicine approaches to prostate cancer screening decisions in diverse populations.
Published: 2021
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25. Circadian genes and risk of prostate cancer: Findings from the EPICAP study

Author: Brigitte Trétarre, Yves Akoli Koudou, Xavier Rebillard, Anne Boland, Geraldine Cancel-Tassin, Olivier Cussenot, Méyomo G. Wendeu-Foyet, Delphine Bacq, Pierre-Jean Lamy, Thérèse Truong, Florence Menegaux, Jean-François Deleuze, Sylvie Cénée, Pierre Laurent-Puig, and Claire Mulot
Subjects: Oncology, Cancer Research, medicine.medical_specialty, education.field_of_study, NPAS2, Circadian clock, Population, Single-nucleotide polymorphism, Biology, medicine.disease, 3. Good health, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, medicine.anatomical_structure, Prostate, 030220 oncology & carcinogenesis, Internal medicine, medicine, Circadian rhythm, education, PER1
Abstract: Circadian rhythms regulate several physiological functions and genes controlling the circadian rhythm were found to regulate cell proliferation, cell cycle and apoptosis. Few studies have investigated the role of those circadian genes in prostate cancer occurrence. We aim to investigate the relationship between circadian genes polymorphisms and prostate cancer risk based on data from the EPICAP study, a population-based case-control study including 1,515 men (732 cases / 783 controls) with genotyped data. Odds Ratios (ORs) for association between prostate cancer and circadian gene variants were estimated for each of the 872 single nucleotide polymorphisms (SNPs) in 31 circadian clock genes. We also used a gene-based and pathway-based approach with a focus on the pathway including 9 core circadian genes. Separate analyses were conducted by prostate cancer aggressiveness. The core-circadian pathway (p = 0.0006) was significantly associated to prostate cancer, for either low (p = 0.002) or high (p = 0.01) grade tumor. At the gene level, we observed significant associations between all prostate cancer and NPAS2 and PER1 after correcting for multiple testing, while only RORA was significant for aggressive tumors. At the SNP-level, no significant association was observed. Our findings provide additional evidence of a potential link between genetic variants in circadian genes and prostate cancer risk. Further investigation is warranted to confirm these findings and to better understand the biological pathways involved.
Published: 2019
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26. Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author: Sara Benlloch, Roger L. Milne, Azad Hassan Abdul Razack, José Manuel Ruiz-Dominguez, Steven Joniau, Maria P. Silva, Martin Andreas Røder, Constance Turman, Anne-Maree Haynes, Jin Ling, Robert N. Hoover, Jong Y. Park, Johanna Schleutker, Brian E. Henderson, Amy Hutchinson, Stephanie J. Weinstein, Manolis Kogevinas, Melissa Papargiris, Monique J. Roobol, Gill Barnett, Wayne D. Tilley, Elio Riboli, Samantha E.T. Larkin, Melissa C. Southey, Michelle Guy, Jeanette T. Bensen, Henrik Grönberg, Fredrick R. Schumacher, Karina Dalsgaard Sørensen, Davor Lessel, Carin Cavalli-Bjoerkman, Tomislav Kuliš, Barry S. Rosenstein, Paula Kujala, Michael Davis, Andrzej M. Kierzek, Antonio Finelli, Gerald L. Andriole, Leire Moya, Antonio Gómez-Caamaño, Demetrius Albanes, Jianming Guo, Lisa F. Newcomb, Koveela Govindasami, Ji Lin, Gert De Meerleer, Manuel Luedeke, Richard M. Martin, Zeljko Kastelan, Kay-Tee Khaw, Ruth C. Travis, Rebecca Elliott, Alexandre R. Zlotta, Xin Guo, Kirsi Talala, Yangling Zhang, Lorelei A. Mucci, Marie Sanchez, Paul D.P. Pharoah, Mariona Bustamante, Peter Klarskov, Aleksandrina Vlahova, Srilakshmi Srinivasan, Aik T. Ong, David E. Neal, Sylvie Cénée, Esther M. John, Sonja I. Berndt, Kan Wang, Peter Iversen, Harry Ostrer, Michael Borre, Freddie C. Hamdy, Christopher A. Haiman, Ji Wu, Florence Menegaux, Jacek Marzec, Sara S. Strom, David P. Dearnaley, Jyotsna Batra, Piet Ost, Mariana C. Stern, Kim De Ruyck, Hyun Soo Park, Trina Yeadon, Elenko Popov, Yudong Wu, Svetlana Christova, Thomas Van den Broeck, Loic Le Marchand, Daniel J. Schaid, Babu Zachariah, Sune F. Nielsen, Mary-Anne Kedda, Judith A. Clements, Olivier Cussenot, Robert Szulkin, Shiro Saito, Andrew Evans, Douglas F. Easton, Gemma Castaño-Vinyals, Steve Hazel, Thérèse Truong, Guomin Wang, Katarina Cuk, Ants Toi, Rosalind A. Eeles, Darina Kachakova, Lourdes Mengual, Lisa G. Horvath, Yuan Chun Ding, Catharine M L West, Ana Carballo, Suzanne K. Chambers, Aurelie Vogt, Angela Cox, Daniel W. Lin, Dominika Wokołorczyk, Manuela Gago-Dominguez, Stephen J. Chanock, Federico Canzian, Aleksandra Klim, Tokhir Dadaev, Kathleen Herkommer, Tihomir Dikov, Lovise Maehle, Jasmine Lim, Janet L. Stanford, Martin Eklund, Guido Jenster, Soo-Hwang Teo, Teemu J. Murtola, Torben F. Ørntoft, Stella Koutros, Christa Stegmaier, Sofia Maia, Mitchell J. Machiela, Lisa A. Cannon-Albright, Clare Berry, Pamela Saunders, Lluís Cecchini, Jeri Kim, Radka Kaneva, Brigitte Trétarre, Anne George, Meir J. Stampfer, Marija Gamulin, Meng H. Tan, Angela Morgan, Jenny L Donovan, Graham G. Giles, Geraldine Cancel-Tassin, Neil Fleshner, Shannon K. McDonnell, Hardeep Ranu, Naomi Livni, Kimmo Taari, Sarah L. Kerns, Csilla Sipeky, Alicja Wolk, Edward Giovannucci, Ninghan Feng, Marta Cardoso, Jan-Erik Johansson, Catherine M. Tangen, Guangwen Cao, Adam S. Kibel, Robert J. MacInnis, Bernd Holleczek, Sarah J Lewis, Bo Zhou, Michael Broms, Maria Elena Martinez, Renea A. Taylor, Børge G. Nordestgaard, Fritz H. Schröder, Ali Amin Al Olama, Sue A. Ingles, Markus Aly, Jie Li, Lori S. Tillmans, Ana Vega, Patricia Calvo, Christopher J. Logothetis, David V. Conti, Miguel Aguado, Inés Gómez-Acebo, Tobias Nordström, Meiling Li, Elaine A. Ostrander, C.H. Bangma, Cyril Fisher, Joanne F. Aitken, Matthew Parliament, Gail P. Risbridger, John L. Hopper, Takashi Imai, Belynda Hicks, Victoria L. Stevens, Cezary Cybulski, G Marsden, Brian D. Carter, Vanessa M. Hayes, Nawaid Usmani, Vanio Mitev, Shan-Chao Zhao, Margaret Cook, Milan S. Geybels, Phyllis J. Goodman, Mark N. Brook, Nora Pashayan, Timothy J. Key, Yongwei Yu, Xavier Rebillard, David J. Hunter, Laura Fachal, Javier Llorca, Afshan Siddiq, Claire Aukim-Hastie, Trinidad Dierssen-Sotos, Walther Vogel, Angel Carracedo, Laura E. Beane Freeman, Julio M. Pow-Sang, Hardev Pandha, Robert A. Gardiner, Shaun M. Riska, Yong-Jie Lu, Zan Sun, Ramón Lobato-Busto, Ami Karlsson, Hongwei Zhang, Guoping Ren, Jing Ma, Huihai Wu, Søren M. Bentzen, John Pedersen, Claire Mulot, Girish S. Kulkarni, Jan Lubinski, Antonio Alcaraz, Jose E. Castelao, Athene Lane, Rasmus Bisbjerg, Thomas A. Sellers, Robert J. Hamilton, Jianfeng Xu, Sofie De Langhe, Artitaya Lophatananon, Maren Weisher, Agnieszka Michael, Yves Akoli Koudou, Niclas Håkansson, Alison M. Dunning, Hubert Thierens, Matthew L. Freedman, Kenneth Muir, Ian M. Thompson, Ian Whitmore, Susan L. Neuhausen, Chavdar Slavov, Wojciech Kluzniak, Laurence N. Kolonel, Lisa M. Butler, Teuvo L.J. Tammela, Alison Thwaites, Theodorus van der Kwast, Liesel M. FitzGerald, Thomas J. Schnoeller, Hermann Brenner, Christiane Maier, Amanda B. Spurdle, Jan Adolfsson, Atanaska Mitkova, Peter Kraft, Paula Peleteiro, Pär Stattin, Xin Sheng, Paul D. Brown, Ron H.N. van Schaik, Zsofia Kote-Jarai, Susan M. Gapstur, Paul A. Townsend, Edward J. Saunders, Bettina F. Drake, Stephen N. Thibodeau, Fredrik Wiklund, Paula Paulo, Esther Gracia-Lavedan, Xueying Mao, Marco Matejcic, Neil G. Burnet, A. L. Eckert, Manuel R. Teixeira, Sara Lindström, Weiyang He, Hui-Yi Lin, Suzanne Kolb, Linda Steele, Philipp Bohnert, Anssi Auvinen, Eli Marie Grindedal, Frank Claessens, and Kathryn L. Penney
Subjects: Urologic Diseases, 0301 basic medicine, Oncology, medicine.medical_specialty, Science, MEDLINE, General Physics and Astronomy, 02 engineering and technology, General Biochemistry, Genetics and Molecular Biology, Germline, 03 medical and health sciences, Internal medicine, medicine, PRACTICAL Consortium, lcsh:Science, Cancer, Prostate cancer risk, Multidisciplinary, business.industry, Prostate Cancer, Published Erratum, General Chemistry, 021001 nanoscience & nanotechnology, medicine.disease, Spelling, 3. Good health, 030104 developmental biology, Variation (linguistics), lcsh:Q, 0210 nano-technology, business
Abstract: The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.
Published: 2019
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27. Circulating Metabolic Biomarkers of Screen-Detected Prostate Cancer in the ProtecT Study

Author: Jeri Kim, Jong Y. Park, Johanna Schleutker, Davor Lessel, Jie Zheng, Rebecca C Richmond, Lovise Maehle, J. Athene Lane, Barry S. Rosenstein, Ana Vega, Robert J. Hamilton, Kim De Ruyck, Richard M. Martin, Graham G. Giles, Sonja I. Berndt, Jyotsna Batra, Manuela Gago Dominguez, Freddie C. Hamdy, Radka Kaneva, Ali Amin Al Olama, Lisa A. Cannon-Albright, Ruth C. Travis, Susan M. Gapstur, Charleen D. Adams, Geraldine Cancel-Tassin, Stephen J. Chanock, Victoria L. Stevens, Lisa F. Newcomb, Diana L. Santos Ferreira, George Davey Smith, David E. Neal, Peter Würtz, Fredrick R. Schumacher, Henrik Grönberg, Manolis Kogevinas, Adam S. Kibel, Christopher A. Haiman, Florence Menegaux, Cezary Cybulski, Sue A. Ingles, Judith A. Clements, Lorelei A. Mucci, Børge G. Nordestgaard, Wes Spiller, Stella Koutros, Nora Pashayan, Karina Dalsgaard Sørensen, David V. Conti, Hardev Pandha, Rosalind A. Eeles, Kay-Tee Khaw, Vanessa Y Tan, Catharine M L West, Sara Benlloch, Christiane Maier, Jenny L Donovan, Azad Hassan Abdul Razack, Catherine M. Tangen, Nawaid Usmani, Yong-Jie Lu, Hermann Brenner, Zsofia Kote-Jarai, Paul A. Townsend, Frank Claessens, Kathryn L. Penney, Demetrius Albanes, Stephen N. Thibodeau, Fredrik Wiklund, Manuel R. Teixeira, Kenneth Muir, Janet L. Stanford, Monique J. Roobol, Susan L. Neuhausen, Alicja Wolk, Caroline L Relton, Esther M. John, and Urology
Subjects: 0301 basic medicine, Oncology, Male, medicine.medical_specialty, Epidemiology, BTC (Bristol Trials Centre), Article, Androgen deprivation therapy, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, SDG 3 - Good Health and Well-being, Prostate, Internal medicine, Mendelian randomization, medicine, Metabolome, Biomarkers, Tumor, Humans, Phospholipids, Triglycerides, Aged, business.industry, Case-control study, Cancer, Prostatic Neoplasms, Mendelian Randomization Analysis, Middle Aged, Prostate-Specific Antigen, medicine.disease, United Kingdom, 3. Good health, Prostate-specific antigen, 030104 developmental biology, medicine.anatomical_structure, Cholesterol, Centre for Surgical Research, 030220 oncology & carcinogenesis, Case-Control Studies, ICEP, business, Genome-Wide Association Study
Abstract: Background: Whether associations between circulating metabolites and prostate cancer are causal is unknown. We report on the largest study of metabolites and prostate cancer (2,291 cases and 2,661 controls) and appraise causality for a subset of the prostate cancer–metabolite associations using two-sample Mendelian randomization (MR). Methods: The case–control portion of the study was conducted in nine UK centers with men ages 50–69 years who underwent prostate-specific antigen screening for prostate cancer within the Prostate Testing for Cancer and Treatment (ProtecT) trial. Two data sources were used to appraise causality: a genome-wide association study (GWAS) of metabolites in 24,925 participants and a GWAS of prostate cancer in 44,825 cases and 27,904 controls within the Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium. Results: Thirty-five metabolites were strongly associated with prostate cancer (P < 0.0014, multiple-testing threshold). These fell into four classes: (i) lipids and lipoprotein subclass characteristics (total cholesterol and ratios, cholesterol esters and ratios, free cholesterol and ratios, phospholipids and ratios, and triglyceride ratios); (ii) fatty acids and ratios; (iii) amino acids; (iv) and fluid balance. Fourteen top metabolites were proxied by genetic variables, but MR indicated these were not causal. Conclusions: We identified 35 circulating metabolites associated with prostate cancer presence, but found no evidence of causality for those 14 testable with MR. Thus, the 14 MR-tested metabolites are unlikely to be mechanistically important in prostate cancer risk. Impact: The metabolome provides a promising set of biomarkers that may aid prostate cancer classification.
Published: 2019
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28. Performance of African-ancestry-specific polygenic hazard score varies according to local ancestry in 8q24

Author: Jennifer Cullen, Brandon A. Mahal, Maria Elena Martinez, Robin J. Leach, Brent S. Rose, Marie-Élise Parent, Catherine M. Tangen, Pascal Blanchet, Tyler M. Seibert, Jong Y. Park, Jennifer J. Hu, Geraldine Cancel-Tassin, Rosalind A. Eeles, Chun Chieh Fan, Esther M. John, Roshan Karunamuni, James L. Mohler, Jack A. Taylor, Melinda C. Aldrich, Artitaya Lophatananon, Luc Multigner, Ole A. Andreassen, Thérèse Truong, Marc Romana, Florence Menegaux, Ian M. Thompson, Laurent Brureau, Kenneth Muir, Olivier Cussenot, Dana C. Crawford, Adam S. Kibel, Gyorgy Petrovics, Asona Lui, Elizabeth T. H. Fontham, Bettina F. Drake, Jeannette T. Bensen, Ian G. Mills, William S. Bush, Hui-Yi Lin, Zsofia Kote-Jarai, Wesley K. Thompson, Maureen Sanderson, Anders M. Dale, Wei Zheng, Jay H. Fowke, Phyllis J. Goodman, William J. Blot, Minh-Phuong Huynh-Le, Collaborators, UKGPCS, Consortium, PRACTICAL, University of California [San Diego] (UC San Diego), University of California, The institute of cancer research [London], Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], Biologie Intégrée du Globule Rouge (BIGR (UMR_S_1134 / U1134)), Institut National de la Transfusion Sanguine [Paris] (INTS)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Université des Antilles (UA)-Université de Paris (UP), This study was funded in part by grants from the University of California (#C21CR2060), the United States National Institute of Health/National Institute of Biomedical Imaging and Bioengineering (#K08EB026503), the Research Council of Norway (#223273), KG Jebsen Stiftelsen, and South East Norway Health Authority., University of California (UC), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Institut National de la Transfusion Sanguine [Paris] (INTS)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Université des Antilles (UA)-Université Paris Cité (UPCité)
Subjects: Male, Multifactorial Inheritance, Cancer Research, Urology, Genetic genealogy, 030232 urology & nephrology, Black People, Single-nucleotide polymorphism, [SDV.CAN]Life Sciences [q-bio]/Cancer, Polymorphism, Single Nucleotide, Risk Assessment, White People, 03 medical and health sciences, 0302 clinical medicine, SDG 3 - Good Health and Well-being, Genotype, Genetic variation, Humans, Medicine, Genetic Predisposition to Disease, 1000 Genomes Project, Prostate cancer risk, Proportional hazards model, business.industry, Prostatic Neoplasms, 3. Good health, Oncology, Case-Control Studies, 030220 oncology & carcinogenesis, Relative risk, business, Chromosomes, Human, Pair 8, Demography
Abstract: Background We previously developed an African-ancestry-specific polygenic hazard score (PHS46+African) that substantially improved prostate cancer risk stratification in men with African ancestry. The model consists of 46 SNPs identified in Europeans and 3 SNPs from 8q24 shown to improve model performance in Africans. Herein, we used principal component (PC) analysis to uncover subpopulations of men with African ancestry for whom the utility of PHS46+African may differ. Materials and methods Genotypic data were obtained from the PRACTICAL consortium for 6253 men with African genetic ancestry. Genetic variation in a window spanning 3 African-specific 8q24 SNPs was estimated using 93 PCs. A Cox proportional hazards framework was used to identify the pair of PCs most strongly associated with the performance of PHS46+African. A calibration factor (CF) was formulated using Cox coefficients to quantify the extent to which the performance of PHS46+African varies with PC. Results CF of PHS46+African was strongly associated with the first and twentieth PCs. Predicted CF ranged from 0.41 to 2.94, suggesting that PHS46+African may be up to 7 times more beneficial to some African men than others. The explained relative risk for PHS46+African varied from 3.6% to 9.9% for individuals with low and high CF values, respectively. By cross-referencing our data set with 1000 Genomes, we identified significant associations between continental and calibration groupings. Conclusion We identified PCs within 8q24 that were strongly associated with the performance of PHS46+African. Further research to improve the clinical utility of polygenic risk scores (or models) is needed to improve health outcomes for men of African ancestry.
Published: 2021
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29. Polygenic hazard score is associated with prostate cancer in multi-ethnic populations

Author: Florence Menegaux, William J. Blot, Henrik Grönberg, Luc Multigner, Sune F. Nielsen, Stella Koutros, Frank Claessens, Manuela Gago-Dominguez, Kathryn L. Penney, Tyler M. Seibert, Cezary Cybulski, Jennifer J. Hu, Hermann Brenner, Radka Kaneva, Sue A. Ingles, Catherine M. Tangen, Ian G. Mills, Janet L. Stanford, Karina Dalsgaard Sørensen, Ruth C. Travis, Marie-Élise Parent, Monique J. Roobol, Nora Pashayan, Jyotsna Batra, Maria Elena Martinez, Anders M. Dale, Wei Zheng, Kay-Tee Khaw, Chad D. Huff, Chun Chieh Fan, Paul A. Townsend, Kim De Ruyck, Yong-Jie Lu, Eli Marie Grindedal, Hardev Pandha, Sonja I. Berndt, Susan L. Neuhausen, Alicja Wolk, Apcb, Wesley K. Thompson, Maureen Sanderson, Demetrius Albanes, Stephen N. Thibodeau, Christiane Maier, Kenneth Muir, Robin J. Leach, Børge G. Nordestgaard, Ole A. Andreassen, Fredrik Wiklund, Graham G. Giles, Zsofia Kote-Jarai, Catharine M L West, Minh-Phuong Huynh-Le, Manolis Kogevinas, Manuel R. Teixeira, Jong Y. Park, Johanna Schleutker, Marija Gamulin, Freddie C. Hamdy, William S. Bush, Barry S. Rosenstein, Stephen Watya, Roshan Karunamuni, Richard M. Martin, Nc-La PCaP Investigators, Ana Vega, Adam S. Kibel, Lisa A. Cannon-Albright, Azad Hassan Abdul Razack, Esther M. John, Christopher J. Logothetis, Jay H. Fowke, Nawaid Usmani, David E. Neal, Canary Pass Investigators, Rosalind A. Eeles, Robert J. Hamilton, Lisa F. Newcomb, Jenny L Donovan, Olivier Cussenot, Lorelei A. Mucci, University of California [San Diego] (UC San Diego), University of California, The institute of cancer research [London], University of Manchester [Manchester], University of Turku, Centre for Cancer Genetic Epidemiology [Cambridge], Department of Oncology-University of Cambridge [UK] (CAM), University College of London [London] (UCL), Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut de recherche en santé, environnement et travail (Irset), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de la Santé et de la Recherche Médicale (INSERM)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université d'Angers (UA), This study was funded in part by a grant from the United States National Institute of Health/National Institute of Biomedical Imaging and Bioengineering (#K08EB026503), United States Department of Defense (#W81XWH-13-1-0391), University of California CRCC C21CR2060, the Research Council of Norway (#223273), K.G. Jebsen Stiftelsen, and South East Norway Health Authority. RM Martin is supported in part by the National Institute for Health Research Bristol Biomedical Research Centre. The CAP trial is funded by Cancer Research UK and the UK Department of Health (C11043/A4286, C18281/A8145, C18281/A11326, C18281/A15064, and C18281/A24432). R.M. Martin was supported by a Cancer Research UK (C18281/A19169) program grant (the Integrative Cancer Epidemiology Programme). Funding for the PRACTICAL consortium member studies is detailed in the Supplementary Information., University of California (UC), University of Cambridge [UK] (CAM)-Department of Oncology, Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Huynh-Le, Minh-Phuong [0000-0002-5025-4709], Fan, Chun Chieh [0000-0001-9437-2128], Eeles, Rosalind A [0000-0002-3698-6241], Muir, Kenneth [0000-0001-6429-988X], Schleutker, Johanna [0000-0002-1863-0305], Pashayan, Nora [0000-0003-0843-2468], Batra, Jyotsna [0000-0003-4646-6247], Grönberg, Henrik [0000-0002-1073-2753], Martin, Richard M [0000-0002-7992-7719], Nordestgaard, Børge G [0000-0002-1954-7220], Wiklund, Fredrik [0000-0002-4623-0544], Giles, Graham G [0000-0003-4946-9099], Wolk, Alicja [0000-0001-7387-6845], Travis, Ruth C [0000-0002-9571-0763], Zheng, Wei [0000-0003-1226-070X], West, Catharine ML [0000-0002-0839-3449], Sørensen, Karina Dalsgaard [0000-0002-4902-5490], Park, Jong Y [0000-0002-6384-6447], Vega, Ana [0000-0002-7416-5137], Teixeira, Manuel R [0000-0002-4896-5982], Multigner, Luc [0000-0003-3205-8568], Cannon-Albright, Lisa [0000-0003-2602-3668], Gamulin, Marija [0000-0003-2431-7910], Bush, William S [0000-0002-9729-6519], Roobol, Monique J [0000-0001-6967-1708], Andreassen, Ole A [0000-0002-4461-3568], Seibert, Tyler M [0000-0002-4089-7399], Apollo - University of Cambridge Repository, and Clinical Chemistry
Subjects: 0301 basic medicine, Oncology, Male, Multifactorial Inheritance, Aging, Multivariate analysis, Ethnic Groups/genetics, General Physics and Astronomy, UKGPCS collaborators, Prostate cancer, 0302 clinical medicine, Urologi och njurmedicin, Ethnicity, risk factors, PRACTICAL Consortium, genetics, Stage (cooking), AgedEthnic Groups / genetics, Cancer, Multidisciplinary, Manchester Cancer Research Centre, Prostatic Neoplasms/genetics, Prostate Cancer, Hazard ratio, APCB, Middle Aged, Hazard, Health equity, 3. Good health, Multidisciplinary Sciences, 030220 oncology & carcinogenesis, Science & Technology - Other Topics, polygenic hazard score (PHS1), prostate cancer, ICEP, Medical Genetics, Urologic Diseases, medicine.medical_specialty, hazard, precision medicine, Science, Prostatic Neoplasms / genetics, [SDV.CAN]Life Sciences [q-bio]/Cancer, Ethnic Groups, survival, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Medical research, SDG 3 - Good Health and Well-being, Internal medicine, NC-LA PCaP Investigators, Genetic model, medicine, Urology and Nephrology, Humans, Neoplasm Invasiveness, Multifactorial Inheritance/genetics, Medicinsk genetik, Aged, Canary PASS Investigators, Science & Technology, IMPACT Study Steering Committee and Collaborators, business.industry, Profile Study Steering Committee, ResearchInstitutes_Networks_Beacons/mcrc, Prostatic Neoplasms, General Chemistry, medicine.disease, Multifactorial Inheritance / genetics, 030104 developmental biology, Multivariate Analysis, Self Report, business, Biomarkers
Abstract: Genetic models for cancer have been evaluated using almost exclusively European data, which could exacerbate health disparities. A polygenic hazard score (PHS1) is associated with age at prostate cancer diagnosis and improves screening accuracy in Europeans. Here, we evaluate performance of PHS2 (PHS1, adapted for OncoArray) in a multi-ethnic dataset of 80,491 men (49,916 cases, 30,575 controls). PHS2 is associated with age at diagnosis of any and aggressive (Gleason score ≥ 7, stage T3-T4, PSA ≥ 10 ng/mL, or nodal/distant metastasis) cancer and prostate-cancer-specific death. Associations with cancer are significant within European (n = 71,856), Asian (n = 2,382), and African (n = 6,253) genetic ancestries (p, A polygenic hazard score (PHS1) improves prostate cancer screening accuracy in European patients. Here, the authors test the performance of a version compatible with OncoArray genotypes (PHS2) in a multi-ethnic dataset and find that it risk-stratifies men for any, aggressive, and fatal prostate cancer.
Published: 2021
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30. Marital Status and Prostate Cancer Incidence: A Pooled Analysis of 12 Case-Control Studies From the PRACTICAL Consortium

Author: Charlotte Salmon, Lixin Song, Kenneth R Muir, Nora Pashayan, Alison M Dunning, Jyostsna Batra, Suzanne Chambers, Janet L Stanford, Elaine A ostrander, Jong Y Park, Hui-Yi Lin, Olivier Cussenot, Geraldine Cancel-Tassin, Florence Menegaux, Emilie Cordina-Duverger, Manolis Kogevinas, Javier Llorca, Radka Kaneva, Azad Razack, Jasmine Lim, Manueal Gago-Dominguez, Jose E Castelao, Zsofia Kote-Jarai, Marie-Elise Parent, and Rosalind Eeles
Abstract: While being in a committed relationship is associated with a better prostate cancer prognosis, little is known about how marital status relates to its incidence. Social support provided by marriage/relationship could promote a healthy lifestyle and an increased healthcare seeking behavior.We investigated the association between marital status and prostate cancer risk using data from the PRACTICAL Consortium. Pooled analyses were conducted combining 12 case-control studies based on histologically-confirmed incident prostate cancers and controls with information on marital status prior to diagnosis/interview. Marital status was categorized as married/partner, separated/divorced, single, or widowed. Tumours with Gleason scores ≥8 defined high-grade cancers, and low-grade otherwise. NCI-SEER’s summary stages (local, regional, distant) indicated the extent of the cancer. Logistic regression was used to derive odds ratios (ORs) and 95% confidence intervals (CI) for the association between marital status and prostate cancer risk, adjusting for potential confounders. Overall, 14,760 cases and 12,019 controls contributed to analyses. Compared to men who were married/with a partner, widowed men had an OR of 1.19 (95%CI 1.03-1.35) of prostate cancer, with little difference between low- and high-grade tumours. Risk estimates among widowers were 1.14 (95%CI 0.97-1.34) for local, 1.53 (95%CI 1.22-1.92) for regional, and 1.56 (95%CI 1.05-2.32) for distant stage tumours. Single men had elevated risks of high-grade cancers. Our findings highlight elevated risks of incident prostate cancer among widowers, more often characterized by tumours that had spread beyond the prostate at the time of diagnosis. Social support interventions and closer medical follow-up in this sub-population are warranted.
Published: 2021
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31. Marital status and prostate cancer incidence: a pooled analysis of 12 case-control studies from the PRACTICAL consortium

Author: Charlotte, Salmon, Lixin, Song, Kenneth, Muir, Nora, Pashayan, Alison M, Dunning, Jyotsna, Batra, Suzanne, Chambers, Janet L, Stanford, Elaine A, Ostrander, Jong Y, Park, Hui-Yi, Lin, Olivier, Cussenot, Géraldine, Cancel-Tassin, Florence, Menegaux, Emilie, Cordina-Duverger, Manolis, Kogevinas, Javier, Llorca, Radka, Kaneva, Chavdar, Slavov, Azad, Razack, Jasmine, Lim, Manuela, Gago-Dominguez, Jose Esteban, Castelao, Zsofia, Kote-Jarai, Rosalind A, Eeles, and Marie-Élise, Parent
Subjects: Male, Marital Status, Divorce, Incidence, Population Surveillance, Humans, Prostatic Neoplasms, Social Support, Single Person, Adenocarcinoma, Marriage, Middle Aged, Aged
Abstract: While being in a committed relationship is associated with a better prostate cancer prognosis, little is known about how marital status relates to its incidence. Social support provided by marriage/relationship could promote a healthy lifestyle and an increased healthcare seeking behavior. We investigated the association between marital status and prostate cancer risk using data from the PRACTICAL Consortium. Pooled analyses were conducted combining 12 case-control studies based on histologically-confirmed incident prostate cancers and controls with information on marital status prior to diagnosis/interview. Marital status was categorized as married/partner, separated/divorced, single, or widowed. Tumours with Gleason scores ≥ 8 defined high-grade cancers, and low-grade otherwise. NCI-SEER's summary stages (local, regional, distant) indicated the extent of the cancer. Logistic regression was used to derive odds ratios (ORs) and 95% confidence intervals (CI) for the association between marital status and prostate cancer risk, adjusting for potential confounders. Overall, 14,760 cases and 12,019 controls contributed to analyses. Compared to men who were married/with a partner, widowed men had an OR of 1.19 (95% CI 1.03-1.35) of prostate cancer, with little difference between low- and high-grade tumours. Risk estimates among widowers were 1.14 (95% CI 0.97-1.34) for local, 1.53 (95% CI 1.22-1.92) for regional, and 1.56 (95% CI 1.05-2.32) for distant stage tumours. Single men had elevated risks of high-grade cancers. Our findings highlight elevated risks of incident prostate cancer among widowers, more often characterized by tumours that had spread beyond the prostate at the time of diagnosis. Social support interventions and closer medical follow-up in this sub-population are warranted.
Published: 2021

32. Performance of African-ancestry-specific polygenic hazard score varies according to local ancestry in 8q24

Author: Marc Romana, Pascal Blanchet, Hui Yi Lin, Catherine M. Tangen, William J. Blot, Florence Menegaux, Marie-Élise Parent, Jennifer Cullen, Robin J. Leach, Geraldine Cancel-Tassin, Wesley Thompson, Adam S. Kibel, Chun Chieh Fan, Melinda C. Aldrich, Artitaya Lophatananon, Kenneth Muir, Minh-Phuong Huynh-Le, Brandon A. Mahal, Ole A. Andreassen, Thérèse Truong, Jong Y. Park, Ian M. Thompson, Dana C. Crawford, Olivier Cussenot, Gyorgy Petrovics, Luc Multigner, Elizabeth T. H. Fontham, James L. Mohler, Maria Elena Martinez, Jay H. Fowke, Jack A. Taylor, Esther M. John, Phyllis J. Goodman, Zsofia Kote-Jarai, Roshan Karunamuni, Maureen Sanderson, Ian G. Mills, Tyler M. Seibert, Jennifer J. Hu, Anders M. Dale, William S. Bush, Wei Zheng, Asona Lui, Bettina F. Drake, Jeannette T. Bensen, Rosalind A. Eeles, Laurent Brureau, and Brent S. Rose
Subjects: 0303 health sciences, Proportional hazards model, Genetic genealogy, Single-nucleotide polymorphism, Biology, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, 030220 oncology & carcinogenesis, Relative risk, Genetic variation, Genotype, SNP, 1000 Genomes Project, 030304 developmental biology, Demography
Abstract: We previously developed an African-ancestry-specific polygenic hazard score (PHS46+African) that substantially improved prostate cancer risk stratification in men with African ancestry. The model consists of 46 SNPs identified in Europeans and 3 SNPs from 8q24 shown to improve model performance in Africans. Herein, we used principal component (PC) analysis to uncover subpopulations of men with African ancestry for whom the utility of PHS46+African may differ. Genotypic data were obtained from PRACTICAL consortium for 6,253 men with African genetic ancestry. Genetic variation in a window spanning 3 African-specific 8q24 SNPs was estimated using 93 PCs. A Cox proportional hazards framework was used to identify the pair of PCs most strongly associated with performance of PHS46+African. A calibration factor (CF) was formulated using estimated Cox coefficients to quantify the extent to which the performance of PHS46+African varies with PC. CF of PHS46+African was strongly associated with the first and twentieth PCs. Predicted CF ranged from 0.41 to 2.94, suggesting that PHS46+African may be up to 7 times more beneficial to some African men than others. The explained relative risk for PHS46+African varied from 3.6% to 9.9% for individuals with low and high CF values, respectively. By cross-referencing our dataset with 1000 Genomes, we identified statistically significant associations between continental and calibration groupings. In conclusion, we identified PCs within 8q24 SNP window that were strongly associated with performance of PHS46+African. Further research to improve clinical utility of polygenic risk scores (or models) is needed to improve health outcomes for men of African ancestry
Published: 2021
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33. Publisher Correction: Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author: Brian D. Carter, Gert De Meerleer, Michael B. Cook, Paul A. Townsend, Kim De Ruyck, Edward J. Saunders, Christopher A. Haiman, Atushi Takahashi, Sonja I. Berndt, Florence Menegaux, Cezary Cybulski, Barbara Nemesure, Loic Le Marchand, Sune F. Nielsen, Demetrius Albanes, Robert J. Hamilton, Ninghan Feng, Stella Koutros, Stephen J. Chanock, Wei Zheng, Thomas A. Sellers, Rick A. Kittles, Craig C. Teerlink, Stephen N. Thibodeau, Marija Gamulin, Artitaya Lophatananon, Niclas Håkansson, Fredrik Wiklund, Roberta McKean-Cowdin, Yuan Chun Ding, Nora Pashayan, Timothy J. Key, Børge G. Nordestgaard, Shannon K. McDonnell, Jong Y. Park, Laura Fachal, Martin Andreas Røder, Johanna Schleutker, Edward Giovannucci, Anssi Auvinen, Hardev Pandha, Maria Elena Martinez, Mitchell J. Machiela, Gill Barnett, Melissa C. Southey, Graham G. Giles, Barry S. Rosenstein, Stephen Watya, Bernd Holleczek, Pascal Blanchet, Agnieszka Michael, William J. Blot, James L. Mohler, Jack A. Taylor, Sarah L. Kerns, Adam S. Kibel, Piet Ost, Ana Vega, Richard M. Martin, Jennifer J. Hu, Nicholas Mancuso, Yukihide Momozawa, Robert J. MacInnis, Sue A. Ingles, Maureen Sanderson, Kai Uwe Saum, Markus Aly, Robert Szulkin, Davor Lessel, Hermann Brenner, Yves Akoli Koudou, Jan Lubinski, Mina Torres, Anselm Hennis, Eli Marie Grindedal, Csilla Sipeky, Susan L. Neuhausen, Alison M. Dunning, Alicja Wolk, Adam B. Murphy, Brandi Weaver, Mariana C. Stern, Paula Paulo, Stephanie J. Weinstein, Xueying Mao, Tobias Nordström, Neil Fleshner, Tokhir Dadaev, Teuvo L.J. Tammela, Jay H. Fowke, Tomislav Kuliš, Steven Joniau, Yudong Wu, Rosalind A. Eeles, Shan Chao Zhao, Kenneth Muir, Mark N. Brook, Hidewaki Nakagawa, Freddie C. Hamdy, Karina Dalsgaard Sørensen, Linda Steele, Alisha Chou, Dominika Wokołorczyk, Peggy Wan, Martin Eklund, Laurent Brureau, Lisa A. Cannon-Albright, Lilit C. Moss, Daniel J. Schaid, Luc Multigner, Benjamin A. Rybicki, Xin Sheng, Constance Turman, Ron H.N. van Schaik, Radka Kaneva, Zsofia Kote-Jarai, Frank Claessens, Katarina Cuk, Kay-Tee Khaw, Chad D. Huff, Henrik Grönberg, Kathryn L. Penney, Geraldine Cancel-Tassin, Eric A. Klein, Masashi Fujita, Jennifer Cullen, Michael Borre, Jenny L Donovan, Dana C. Crawford, Antonio Gómez-Caamaño, David V. Conti, Manuel Luedeke, Maya Ghoussaini, Janet L. Stanford, Peter Kraft, Ian M. Thompson, Koichi Matsuda, Soo-Hwang Teo, Christopher J. Logothetis, Robin J. Leach, Monique J. Roobol, Manuel R. Teixeira, Jose Esteban Castelao, Sara S. Strom, Vanio Mitev, Stig E. Bojesen, David J. Hunter, Wayne D. Tilley, Jyotsna Batra, Gerald L. Andriole, Christine Neslund-Dudas, Sara Lindström, Guido Jenster, Catherine M. Tangen, William S. Bush, Maren Weischer, Chavdar Slavov, Thomas J. Schnoeller, Javier Llorca, Claire Aukim-Hastie, Nawaid Usmani, Lisa G. Horvath, Daniel W. Lin, Esther M. John, Burcu F. Darst, Milan S. Geybels, Phyllis J. Goodman, Lynne R. Wilkens, Ali Amin Al Olama, Lorelei A. Mucci, Peter Iversen, Christiane Maier, Victoria L. Stevens, Andreia Brandão, Graham Casey, Neil G. Burnet, Ann W. Hsing, Hongwei Zhang, Laura E. Beane Freeman, Susan M. Gapstur, Sara Benlloch, James E. Mensah, Marie-Élise Parent, Jianfeng Xu, Bettina F. Drake, Jeannette T. Bensen, Azad Hassan Abdul Razack, Edward D. Yeboah, David E. Neal, John D. Carpten, Ruth C. Travis, Thomas J. Hoffmann, Thomas Van den Broeck, Jeri Kim, Ali Sahimi, Gemma Castaño-Vinyals, Alexander Lubwama, Leire Moya, Elio Riboli, Douglas F. Easton, Suzanne K. Chambers, Yong-Jie Lu, Melinda C. Aldrich, Manuela Gago-Dominguez, John S. Witte, Matthew Parliament, Gail P. Risbridger, Samantha E.T. Larkin, Lisa F. Newcomb, Fredrick R. Schumacher, Shiv Srivastava, Jasmine Lim, Meir J. Stampfer, Harry Ostrer, Judith A. Clements, Thérèse Truong, Catharine M L West, Zan Sun, Olivier Cussenot, Gyorgy Petrovics, Lovise Maehle, Elizabeth T. H. Fontham, William B. Isaacs, Hui Yi Lin, Rohit Varma, Elaine A. Ostrander, Manolis Kogevinas, Robert N. Hoover, Sandeep Singhal, Antonio Finelli, and Stephen K. Van Den Eeden
Subjects: 0303 health sciences, business.industry, Published Erratum, MEDLINE, Genome-wide association study, Computational biology, Biology, medicine.disease, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Meta-analysis, Genetics, medicine, Susceptibility locus, 06 Biological Sciences, 11 Medical and Health Sciences, Personalized medicine, Genetic risk, business, 030217 neurology & neurosurgery, 030304 developmental biology, Developmental Biology
Abstract: In the version of this article originally published, the names of the equally contributing authors and jointly supervising authors were switched. The correct affiliations are: “These authors contributed equally: David V. Conti, Burcu F. Darst. These authors jointly supervised this work: David V. Conti, Rosalind A. Eeles, Zsofia Kote-Jarai, Christopher A. Haiman.” The error has been corrected in the HTML and PDF versions of the article.
Published: 2021

34. Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author: Paul A. Townsend, Edward J. Saunders, Hidewaki Nakagawa, Manuel R. Teixeira, Graham Casey, Demetrius Albanes, Christine Neslund-Dudas, Sara Lindström, William S. Bush, Maren Weischer, Lisa A. Cannon-Albright, Rick A. Kittles, Peggy Wan, Martin Eklund, Stephen N. Thibodeau, Burcu F. Darst, Fredrik Wiklund, Nicholas Mancuso, Jeri Kim, Jong Y. Park, Johanna Schleutker, Maureen Sanderson, Samantha E.T. Larkin, Radka Kaneva, Hongwei Zhang, Daniel J. Schaid, Luc Multigner, Marie-Élise Parent, Robert Szulkin, Fredrick R. Schumacher, Geraldine Cancel-Tassin, Jianfeng Xu, Gill Barnett, Melissa C. Southey, Yuan Chun Ding, Alexander Lubwama, Maria Elena Martinez, Manolis Kogevinas, Linda Steele, Laurent Brureau, Shiv Srivastava, Maya Ghoussaini, Alison M. Dunning, Adam B. Murphy, Kenneth Muir, Edward Giovannucci, Mitchell J. Machiela, James L. Mohler, Jack A. Taylor, Robert N. Hoover, Sandeep Singhal, Chavdar Slavov, Guido Jenster, Frank Claessens, Neil Fleshner, Sara Benlloch, Gert De Meerleer, Michael B. Cook, Zan Sun, Harry Ostrer, Pascal Blanchet, Lynne R. Wilkens, Ali Amin Al Olama, Sue A. Ingles, Markus Aly, Jay H. Fowke, Agnieszka Michael, Yves Akoli Koudou, Victoria L. Stevens, Kathryn L. Penney, Ana Vega, Xin Sheng, Ron H.N. van Schaik, Zsofia Kote-Jarai, Kim De Ruyck, Christopher A. Haiman, Atushi Takahashi, Florence Menegaux, Judith A. Clements, Stephen K. Van Den Eeden, Brian D. Carter, Wayne D. Tilley, Antonio Finelli, Jennifer J. Hu, Hermann Brenner, Thomas Van den Broeck, Shan Chao Zhao, Azad Hassan Abdul Razack, Edward D. Yeboah, Sonja I. Berndt, Barbara Nemesure, Mark N. Brook, David V. Conti, Katarina Cuk, Teuvo L.J. Tammela, Ali Sahimi, Stephen J. Chanock, Loic Le Marchand, Gemma Castaño-Vinyals, Sune F. Nielsen, Sara S. Strom, Ann W. Hsing, Roberta McKean-Cowdin, David J. Hunter, Ian M. Thompson, Børge G. Nordestgaard, Jyotsna Batra, Paula Paulo, Masashi Fujita, Jennifer Cullen, Susan M. Gapstur, Sarah L. Kerns, Lorelei A. Mucci, Neil G. Burnet, Xueying Mao, Hui Yi Lin, Rohit Varma, Marija Gamulin, Wei Zheng, Thomas A. Sellers, Adam S. Kibel, Robert J. Hamilton, Leire Moya, Ninghan Feng, Laura E. Beane Freeman, James E. Mensah, Catherine M. Tangen, Shannon K. McDonnell, Matthew Parliament, Davor Lessel, Gail P. Risbridger, Mina Torres, Janet L. Stanford, Bettina F. Drake, Soo-Hwang Teo, Robert J. MacInnis, Stig E. Bojesen, Jeannette T. Bensen, William J. Blot, Stella Koutros, Robin J. Leach, Graham G. Giles, Piet Ost, Artitaya Lophatananon, Laura Fachal, Tomislav Kuliš, Peter Kraft, Monique J. Roobol, Elaine A. Ostrander, Niclas Håkansson, Anselm Hennis, Yukihide Momozawa, Anssi Auvinen, Koichi Matsuda, Steven Joniau, Lisa G. Horvath, Javier Llorca, Claire Aukim-Hastie, Bernd Holleczek, Daniel W. Lin, Gerald L. Andriole, John D. Carpten, Eli Marie Grindedal, Rosalind A. Eeles, Elio Riboli, Constance Turman, Martin Andreas Røder, Yong-Jie Lu, Tobias Nordström, Kai Uwe Saum, Esther M. John, Melinda C. Aldrich, Peter Iversen, Henrik Grönberg, John S. Witte, Andreia Brandão, Eric A. Klein, Olivier Cussenot, Barry S. Rosenstein, Stephen Watya, Jan Lubinski, Douglas F. Easton, Dana C. Crawford, Gyorgy Petrovics, Thomas J. Schnoeller, Richard M. Martin, Stephanie J. Weinstein, Jose Esteban Castelao, Suzanne K. Chambers, Tokhir Dadaev, Karina Dalsgaard Sørensen, Antonio Gómez-Caamaño, Lisa F. Newcomb, Csilla Sipeky, Lovise Maehle, Brandi Weaver, Susan L. Neuhausen, Christiane Maier, Alicja Wolk, Vanio Mitev, Thérèse Truong, Manuel Luedeke, Jenny L Donovan, Mariana C. Stern, Catharine M L West, Manuela Gago-Dominguez, Elizabeth T. H. Fontham, William B. Isaacs, David E. Neal, Christopher J. Logothetis, Alisha Chou, Jasmine Lim, Benjamin A. Rybicki, Kay-Tee Khaw, Meir J. Stampfer, Chad D. Huff, Thomas J. Hoffmann, Michael Borre, Freddie C. Hamdy, Nawaid Usmani, Cezary Cybulski, Craig C. Teerlink, Milan S. Geybels, Nora Pashayan, Timothy J. Key, Phyllis J. Goodman, Hardev Pandha, Ruth C. Travis, Yudong Wu, Dominika Wokołorczyk, Lilit C. Moss, University of Southern California (USC), Keck School of Medicine [Los Angeles], CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], The institute of cancer research [London], U01CA194393, National Institutes of Health, NA, Achievement Rewards for College Scientists Foundation, Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de la Santé et de la Recherche Médicale (INSERM)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université d'Angers (UA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Urology, Clinical Chemistry, Darst, Burcu F [0000-0002-6205-4632], Chou, Alisha [0000-0001-7521-6373], Schumacher, Fredrick R [0000-0002-3073-7463], Dadaev, Tokhir [0000-0002-8268-0438], Brook, Mark N [0000-0002-8969-2378], Hoffmann, Thomas J [0000-0001-6893-4449], Takahashi, Atushi [0000-0001-7099-8767], Matsuda, Koichi [0000-0001-7292-2686], Fujita, Masashi [0000-0002-1457-6233], Muir, Kenneth [0000-0001-6429-988X], Stevens, Victoria L [0000-0003-0259-4407], Schleutker, Johanna [0000-0002-1863-0305], Sipeky, Csilla [0000-0002-8853-4722], Auvinen, Anssi [0000-0003-1125-4818], Giles, Graham G [0000-0003-4946-9099], Martin, Richard M [0000-0002-7992-7719], Nordestgaard, Børge G [0000-0002-1954-7220], Bojesen, Stig E [0000-0002-4061-4133], Røder, Martin Andreas [0000-0002-0019-5333], Batra, Jyotsna [0000-0003-4646-6247], Tilley, Wayne [0000-0003-1893-2626], Risbridger, Gail P [0000-0003-3089-4028], Gronberg, Henrik [0000-0002-1073-2753], Eklund, Martin [0000-0001-5032-5266], Nordström, Tobias [0000-0003-4915-7546], Pashayan, Nora [0000-0003-0843-2468], Dunning, Alison M [0000-0001-6651-7166], Travis, Ruth C [0000-0002-9571-0763], Riboli, Elio [0000-0001-6795-6080], Park, Jong Y [0000-0002-6384-6447], Weinstein, Stephanie J [0000-0002-3834-1535], Kraft, Peter [0000-0002-4472-8103], Ostrander, Elaine A [0000-0001-6075-9738], Wolk, Alicja [0000-0001-7387-6845], Håkansson, Niclas [0000-0001-7673-5554], Machiela, Mitchell J [0000-0001-6538-9705], Sørensen, Karina Dalsgaard [0000-0002-4902-5490], Zheng, Wei [0000-0003-1226-070X], Mensah, James E [0000-0003-4133-1722], Lu, Yong-Jie [0000-0001-6174-6621], West, Catharine ML [0000-0002-0839-3449], Cancel-Tassin, Géraldine [0000-0002-9583-6382], Truong, Thérèse [0000-0002-2943-6786], Vega, Ana [0000-0002-7416-5137], Gómez-Caamaño, Antonio [0000-0002-9773-4590], Fachal, Laura [0000-0002-7256-9752], Kerns, Sarah L [0000-0002-6503-0011], Ostrer, Harry [0000-0002-2209-5376], Teixeira, Manuel R [0000-0002-4896-5982], Brandão, Andreia [0000-0003-0938-1543], Cannon-Albright, Lisa [0000-0003-2602-3668], Multigner, Luc [0000-0003-3205-8568], Klein, Eric A [0000-0002-1783-0698], Murphy, Adam B [0000-0001-9977-3473], Michael, Agnieszka [0000-0002-7262-6227], Ost, Piet [0000-0002-2203-4848], Xu, Jianfeng [0000-0002-1343-8752], Teo, Soo-Hwang [0000-0002-0444-590X], Lessel, Davor [0000-0003-4496-244X], Kulis, Tomislav [0000-0002-0895-5691], Joniau, Steven [0000-0003-3195-9890], Bush, William S [0000-0002-9729-6519], Crawford, Dana C [0000-0002-6437-6248], Roobol, Monique J [0000-0001-6967-1708], Jenster, Guido [0000-0002-8658-2552], Van Den Eeden, Stephen K [0000-0002-5599-8387], Easton, Douglas F [0000-0003-2444-3247], Chanock, Stephen J [0000-0002-2324-3393], Wiklund, Fredrik [0000-0002-4623-0544], Eeles, Rosalind A [0000-0002-3698-6241], Haiman, Christopher A [0000-0002-0097-9971], and Apollo - University of Cambridge Repository
Subjects: Male, 8Q24, Genome-wide association study, Continental Population Groups/genetics, VARIANTS, Prostate cancer, 0302 clinical medicine, Risk Factors, Epidemiology, IMPUTATION, Odds Ratio, Prostatic Neoplasms/diagnosis, 0303 health sciences, education.field_of_study, Continental Population Groups, Manchester Cancer Research Centre, Middle Aged, Càncer--Aspectes genètics, 3. Good health, ODDS RATIOS, 06 Biological Sciences, 11 Medical and Health Sciences, medicine.medical_specialty, Population, Biology, prostate cancer, meta-analysis, SEQUENCE, Article, 03 medical and health sciences, Breast cancer, SDG 3 - Good Health and Well-being, Genetics, medicine, BREAST-CANCER, Humans, Genetic Predisposition to Disease, Neoplasm Invasiveness, education, 030304 developmental biology, Genetic association, [SDV.GEN]Life Sciences [q-bio]/Genetics, MUTATIONS, ResearchInstitutes_Networks_Beacons/mcrc, Racial Groups, Prostatic Neoplasms, Molecular Sequence Annotation, Odds ratio, medicine.disease, BRCA2, Pròstata--Càncer, Genetic Loci, 030217 neurology & neurosurgery, Imputation (genetics), Genètica, Demography, Developmental Biology, Genome-Wide Association Study
Abstract: International audience; Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.
Published: 2021
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35. African-specific improvement of a polygenic hazard score for age at diagnosis of prostate cancer

Author: Ian M. Thompson, Roshan Karunamuni, Elizabeth T.H. Fontham, Tyler M. Seibert, Jennifer J. Hu, Jong Y. Park, Phyllis J. Goodman, Ian G. Mills, Luc Multigner, James L. Mohler, Jack A. Taylor, Anders M. Dale, Wei Zheng, Chun Fan, Bettina F. Drake, Jeannette T. Bensen, Florence Menegaux, Supriya Srivastava, Laurent Brureau, Wesley K. Thompson, Hui Yi Lin, Jay H. Fowke, Maureen Sanderson, Zsofia Kote-Jarai, Rosalind A. Eeles, Geraldine Cancel-Tassin, William Blot, Minh-Phuong Huynh-Le, Catherine M. Tangen, Melinda C. Aldrich, Olivier Cussenot, Gyorgy Petrovics, Ole A. Andreassen, Thérèse Truong, Jennifer Cullen, Robin J. Leach, Esther M. John, Artitaya Lophatananon, Pascal Blanchet, Marc Romana, Kenneth Muir, William S. Bush, Marie-Élise Parent, Dana C. Crawford, Adam S. Kibel, University of California [San Diego] (UC San Diego), University of California (UC), Healthlytix [San Diego], The Royal Marsden, The institute of cancer research [London], University of Manchester [Manchester], University of Warwick [Coventry], Fred Hutchinson Cancer Research Center [Seattle] (FHCRC), Vanderbilt University School of Engineering [Nashville] (VUSE), GeneDx [Gaithersburg, MD, USA], Brigham & Women’s Hospital [Boston] (BWH), Harvard Medical School [Boston] (HMS), Washington University in Saint Louis (WUSTL), Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, H. Lee Moffitt Cancer Center and Research Institute, Louisiana State University (LSU), University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC), National Institute of Environmental Health Sciences [Durham] (NIEHS-NIH), National Institutes of Health [Bethesda] (NIH), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Biologie Intégrée du Globule Rouge (BIGR (UMR_S_1134 / U1134)), Institut National de la Transfusion Sanguine [Paris] (INTS)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Université des Antilles (UA)-Université Paris Cité (UPCité), The University of Texas at San Antonio (UTSA), Stanford University, Vanderbilt University [Nashville], Case Western Reserve University [Cleveland], eResearch Collaboratory [Quebec City], McGill University = Université McGill [Montréal, Canada], University of Miami Leonard M. Miller School of Medicine (UMMSM), School of Medicine, Dentistry and Biomedical Sciences [Belfast], Queen's University [Belfast] (QUB), University of Oslo (UiO), KG Jebsen Stiftelsen, National Institute of Biomedical Imaging and BioengineeringUnited States Department of Health and Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Biomedical Imaging and Bioengineering (NIBIB) [K08EB026503], Research Council of NorwayResearch Council of Norway [223273], South East Norway Health Authority, U.S. Department of DefenseUnited States Department of Defense [W81XWH-13-1-0391], Chard-Hutchinson, Xavier, collaborators, UKGPCS, Consortium, PRACTICAL, University of California, Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de la Santé et de la Recherche Médicale (INSERM)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université d'Angers (UA), and Institut National de la Transfusion Sanguine [Paris] (INTS)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Université des Antilles (UA)-Université de Paris (UP)
Subjects: Male, Cancer Research, Multifactorial Inheritance, Genotyping Techniques, [SDV]Life Sciences [q-bio], Age at diagnosis, Genome-wide association study, Prostate cancer, 0302 clinical medicine, Genotype, genome wide association study, 0303 health sciences, education.field_of_study, genotypic ancestry, Age Factors, Middle Aged, prostate cancer, Hazard, [SDV] Life Sciences [q-bio], Oncology, 030220 oncology & carcinogenesis, polygenic risk, Genetic genealogy, Population, Black People, Single-nucleotide polymorphism, [SDV.CAN]Life Sciences [q-bio]/Cancer, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, SDG 3 - Good Health and Well-being, medicine, genomics, Humans, Genetic Predisposition to Disease, education, Proportional Hazards Models, 030304 developmental biology, Genetic association, health disparities, Models, Genetic, Proportional hazards model, business.industry, African, Prostatic Neoplasms, medicine.disease, Case-Control Studies, business, Demography
Abstract: IntroductionPolygenic hazard score (PHS) models are associated with age at diagnosis of prostate cancer. Our model developed in Europeans (PHS46), showed reduced performance in men with African genetic ancestry. We used a cross-validated search to identify SNPs that might improve performance in this population.Material and MethodsAnonymized genotypic data were obtained from the PRACTICAL consortium for 6,253 men with African genetic ancestry. Ten iterations of a ten-fold cross-validation search were conducted, to select SNPs that would be included in the final PHS46+African model. The coefficients of PHS46+African were estimated in a Cox proportional hazards framework using age at diagnosis as the dependent variable and PHS46, and selected SNPs as predictors. The performance of PHS46 and PHS46+African were compared using the same cross-validated approach.ResultsThree SNPs (rs76229939, rs74421890, and rs5013678) were selected for inclusion in PHS46+African. All three SNPs are located on chromosome 8q24. PHS46+African showed substantial improvements in all performance metrics measured, including a 75% increase in the relative hazard of those in the upper 20% compared to the bottom 20% (2.47 to 4.34) and a 20% reduction in the relative hazard of those in the bottom 20% compared to the middle 40% (0.65 to 0.53).ConclusionsWe identified three SNPs that substantially improved the association of PHS46 with age at diagnosis of prostate cancer in men with African genetic ancestry to levels comparable to Europeans and Asians. A strategy of building on established statistical models might benefit ancestral groups generally under-represented in genome-wide association studies.
Published: 2021
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36. Impact on Quality of Life 3 Years After Diagnosis of Prostate Cancer Patients: An Observational Case-Control Study

Author: Xavier Rebillard, Nadine Houédé, Florence Menegaux, Sarah Kabani, Sophie Bouvet, Brigitte Trétarre, and Pascale Fabbro-Peray
Subjects: medicine.medical_specialty, Prostate cancer, Quality of life (healthcare), business.industry, Case-control study, Medicine, Observational study, business, Intensive care medicine, medicine.disease
Abstract: Background Prostate cancer patients are known to suffer from poor sexual and urinary long-term side-effects following treatment, potentially impacting quality of life. The purpose of our study was to compare health-related quality of life at 3 years between prostate cancer patients and healthy controls according to key life-style characteristics. Secondary objectives were to compare urological dysfunction, sexual function, anxiety and depression.Methods Multicentric, case-control, observational prospective, open, follow-up study including 819 prostate cancer patients Results In total, 564 participants were included (mean age 67.9 years): 376 patients and 188 controls. Treatment breakdown was: 258 underwent RP, 90 received EBRT, 52 brachytherapy or HIFU, 15 CT, 26 ADT and 61 AS. There was no difference in median global quality of life between patients and controls (94.87 vs 94.15, p = 0.71). Multivariate analysis showed poorer social functioning in patients (24.3% vs. 16.3%, p = 0.0209), more dyspnea (22% vs. 12.4%, p = 0.0078), and yet less current pain (23% vs 33%, p = 0.0151).Conclusions Global health status score at 3 years after diagnosis was similar between patients and controls, though patients showed a significantly worse social functioning. Prostate cancer diagnosis per se does not impact the quality of life of patients. However, the therapeutic option that will be chosen following diagnosis should be carefully discussed with the medical staff in terms of benefit-risk ratios as it could have a long-term impact on urinary or erectile dysfunction.Trial registration: clinicaltrials.gov, NCT02854982. Registered 4 August 2016 – retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02854982
Published: 2020
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37. Impact on quality of life 3 years after diagnosis of prostate cancer patients below 75 at diagnosis: an observational case-control study

Author: Xavier Rebillard, Nadine Houede, Sophie Bouvet, Brigitte Trétarre, Florence Menegaux, Sarah Kabani, Pascale Fabbro-Peray, Institut de Recherche en Cancérologie de Montpellier (IRCM - U1194 Inserm - UM), CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Clinique Beau Soleil [Montpellier], Laboratoire de Biostatistique, Epidémiologie clinique, Santé Publique Innovation et Méthodologie [CHU Nîmes] (BESPIM), Hôpital Universitaire Carémeau [Nîmes] (CHU Nîmes), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Institut du Cancer de Montpellier (ICM), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, and ONOFRE, Mélanie
Subjects: Extracorporeal Shockwave Therapy, Male, 0301 basic medicine, Cancer Research, Time Factors, medicine.medical_treatment, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Cohort Studies, Androgen deprivation therapy, Prostate cancer, 0302 clinical medicine, Erectile Dysfunction, Quality of life, Surveys and Questionnaires, Prospective Studies, Side effects, Prostatectomy, Middle Aged, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, 3. Good health, Long term survival, Oncology, 030220 oncology & carcinogenesis, Cohort, Urinary dysfunction, Research Article, medicine.medical_specialty, Brachytherapy, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, lcsh:RC254-282, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Internal medicine, Genetics, medicine, Humans, Watchful Waiting, Aged, Radiotherapy, business.industry, Prostatic Neoplasms, Androgen Antagonists, medicine.disease, Health Surveys, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, 030104 developmental biology, Erectile dysfunction, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Case-Control Studies, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, business, Sexual function
Abstract: Background Prostate cancer patients are known to suffer from poor sexual and urinary long-term side-effects following treatment, potentially impacting quality of life. The purpose of our study was to compare health-related quality of life at 3 years between prostate cancer patients and healthy controls according to key life-style characteristics. Secondary objectives were to compare urological dysfunction, sexual function, anxiety and depression. Methods Multicentric, case-control, observational prospective, open, follow-up study including 819 prostate cancer patients Results In total, 564 participants were included (mean age 67.9 years): 376 patients and 188 controls. Treatment breakdown was: 258 underwent RP, 90 received EBRT, 52 brachytherapy or HIFU, 15 CT, 26 ADT and 61 AS. There was no difference in median global quality of life between patients and controls (94.87 vs 94.15, p = 0.71). Multivariate analysis showed poorer social functioning in patients (24.3% vs. 16.3%, p = 0.0209), more dyspnea (22% vs. 12.4%, p = 0.0078), and yet less current pain (23% vs 33%, p = 0.0151). Conclusions Global health status score at 3 years after diagnosis was similar between patients and controls, though patients showed a significantly worse social functioning. Prostate cancer diagnosis per se does not seem to impact the quality of life of patients Trial registration clinicaltrials.gov, NCT02854982. Registered 4 August 2016, retrospectively registered.
Published: 2020
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38. Circadian genes polymorphisms, night work and prostate cancer risk: Findings from the EPICAP study

Author: Sylvie Cénée, Anne Boland, Florence Menegaux, Brigitte Trétarre, Pierre Laurent-Puig, Robert Olaso, Xavier Rebillard, Claire Mulot, Hélène Blanché, Pierre-Jean Lamy, Jean-François Deleuze, Thérèse Truong, Geraldine Cancel-Tassin, Olivier Cussenot, Méyomo G. Wendeu-Foyet, Yves Akoli Koudou, Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Registre des tumeurs de l'Hérault, CRISAP-LR, COLRIM, EPC du CRLC-Centres privés de radiothérapie de l'Hérault-Laboratoires d'Hématologie CPAM - MSA - Caisse militaire, Clinique Beau Soleil [Montpellier], Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), Service d'urologie [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université - Département de santé publique, Centre National de Recherche en Génomique Humaine [Évry] (CNRGH), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Centre d'Etude du Polymorphisme Humain (CEPH), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Fondation Jean Dausset-Université de Paris (UP), Labosud, Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Agence Nationale de Sécurité Sanitaire de l’Alimentation, de l’Environnement et du Travail, ANSES Ligue Contre le Cancer Fondation ARC pour la Recherche sur le Cancer, ARC Ligue Contre le Cancer Agence Française de Sécurité Sanitaire de l'Environnement et du Travail, AFSSET Institut National Du Cancer, INCa Fondation de France, We would like to thank the clinical research nurses who were in charge of participants’ interview, anthropometric measurements and biological sample collection (Anne‐Laure Astolfi, Coline Bernard, Oriane Boyer, Marie‐Hélène De Campo, Sandrine Margaroli, Louise N'Diaye, Sabine Perrier‐Bonnet). We also would like to thank Christian Prad and Nadine Soller for help with patient medical data collection within the Hérault Cancer Registry (Registre des tumeurs de l'Hérault, Montpellier, France) and Cécile Gaffory and Valérie Ondet for technical assistance (CeRePP). Finally, we are grateful to the EPICAP study Group: Urologists: Drs Didier Ayuso, Bruno Ségui, Vincent Abd El Fattah (Centre Hospitalier Bassin de Thau, Sète, France), Alain Guillaume, Jean‐Paul Constans, Olivier Delbos, Pierre Lanfray, Damien Rizet, Etienne Cuénant (Cabinet Urologie du Polygone, Montpellier, France), Michel Locci (Centre Hospitalier, Béziers, France), Etienne Cuénant (Clinique Ste Thérèse, Sète, France), Nicolas Drianno, Bernard Marc, Paulo Soares (Polyclinique Saint Privat, Béziers, France), Antoine Faix, Samer Abdel Hamid, Bruno Ségui (Service urologie, Clinique Beau Soleil, Montpellier, France), Samer Abdel Hamid (Clinique Saint Louis, Ganges, France), Thibaut Murez, Grégoire Poinas, Laurent Cabaniols, Maxime Robert, Rodolphe Thuret (Centre Hospitalo‐Universitaire, Hôpital Lapeyronie, Montpellier, France). Pathologists: Drs Didier Brel, Lysiane Schweizer, Philippe Nayraud, C. Lecam‐Savin (Inopath‐Biomed 34), Roland Daniel, Jean Baptiste Perdigou, Chantal Compan, Mireille Granier, Agnès Grranier, Ruth Borges‐Reis, Alena Badsi, Jean Louis Bouzigues, Elisabeth Broquerie (Inopath‐Labosud) Joëlle Simony, Frédéric Bibeau, Pierre Baldet, Isabelle Serre, Valérie Costes (Centre Hospitalo‐Universitaire, Hôpital Lapeyronie, Montpellier), Marie Laure Gaume (Sète). Biologists: Drs F. Montels (Service de Biologie Médicale, Institut du Cancer de Montpellier, Montpellier, France) and Labosud laboratories: Drs François et Pascal Dumas (Béziers, France), Martine Buono (Sète, France), Isabelle Bonnefille (Lodeve, France), Georges Ruiz (Lunel, France), Didier Paleirac (Clermont‐l'Hérault, France). The EPICAP‐chrono project was funded by Institut National du Cancer, Fondation ARC and Ligue nationale contre le cancer. The EPICAP study was funded by Ligue nationale contre le cancer, Ligue contre le cancer du Val de Marne, Fondation de France, Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES). The first author has been granted by a Paris‐Sud University doctoral allowance., Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), and Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Fondation Jean Dausset-Université Paris Cité (UPCité)
Subjects: Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Genotyping Techniques, Population, interaction, Nerve Tissue Proteins, [SDV.CAN]Life Sciences [q-bio]/Cancer, night work, Polymorphism, Single Nucleotide, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Circadian Clocks, Internal medicine, Basic Helix-Loop-Helix Transcription Factors, medicine, Humans, SNP, Genetic Predisposition to Disease, Circadian rhythm, education, Aged, education.field_of_study, NPAS2, business.industry, ARNTL Transcription Factors, Prostatic Neoplasms, Shift Work Schedule, Cancer, Nuclear Receptor Subfamily 1, Group F, Member 1, Odds ratio, Middle Aged, medicine.disease, prostate cancer, 3. Good health, pathway analysis, ARNTL, Logistic Models, Case-Control Studies, 030220 oncology & carcinogenesis, Neoplasm Grading, business, polymorphisms, circadian genes
Abstract: International audience; Over the past two decades, several studies have attempted to understand the hypothesis that disrupting the circadian rhythm may promote the development of cancer. Some have suggested that night work and some circadian genes polymorphisms are associated with cancer, including prostate cancer. Our study aims to test the hypothesis that prostate cancer risk among night workers may be modulated by genetic polymorphisms in the circadian pathway genes based on data from the EPICAP study, a population-based case-control study including 1511 men (732 cases/779 controls) with genotyped data. We estimated odds ratio (ORs) and P values of the association between prostate cancer and circadian gene variants using logistic regression models. We tested the interaction between circadian genes variants and night work indicators that were significantly associated with prostate cancer at pathway, gene and SNP levels. Analyses were also stratified by each of these night work indicators and by cancer aggressiveness. The circadian pathway was significantly associated with aggressive prostate cancer among night workers (P =.004), particularly for men who worked at night for 10 hours, P =.001). At the gene level, we observed among night workers significant associations between aggressive prostate cancer and ARNTL, NPAS2 and RORA. At the SNP-level, no significant association was observed. Our findings provide some clues of a potential modulating effect of circadian genes in the relationship between night work and prostate cancer. Further investigation is warranted to confirm these findings and to better elucidate the biological pathways involved.
Published: 2020
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39. Body mass index trajectories and prostate cancer risk: Results from the EPICAP study

Author: Florence Menegaux, Emilie Cordina Duverger, Fanny Artaud, C Lavalette, Brigitte Trétarre, Sylvie Cénée, Pierre-Jean Lamy, Xavier Rebillard, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Clinique Beau Soleil [Montpellier], Labosud, Registre des Tumeurs de l'Hérault, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Agence Nationale de Sécurité Sanitaire de l’Alimentation, de l’Environnement et du Travail, ANSES Fondation de France Ligue Contre le Cancer Centre hospitalier universitaire Sainte-Justine, CHUSJ Ligue Contre le Cancer, and The authors thank the clinical research nurses who were in charge of participants' interview, anthropometric measurements and biological sample collection (Anne-Laure Astolfi, Coline Bernard, Oriane Boyer, Marie-H?l?ne De Campo, Sandrine Margaroli, Louise N'Diaye, Sabine Perrier-Bonnet). The authors also thank Christian Prad and Nadine Soller for help with patient medical data collection within the H?rault Cancer Registry (Registre des tumeurs de l'H?rault, Montpellier, France). The authors thank the EPICAP study Group: Urologists: Drs Didier Ayuso, Bruno Segui (Centre Hospitalier Bassin de Thau, S?te, France), Alain Guillaume, Jean-Paul Constans, Olivier Delbos, Pierre Lanfray, Damien Rizet, Etienne Cu?nant?(Cabinet Urologie du Polygone, Montpellier, France), Michel?Locci (Centre Hospitalier, B?ziers, France), Etienne Cu?nant?(Clinique Ste Th?r?se, S?te, France), Nicolas Drianno, Bernard Marc, Paulo Soares (Polyclinique Saint Privat, B?ziers, France), Antoine Faix, Samer Abdel Hamid, Bruno Segui (Service urologie, Clinique Beau Soleil, Montpellier, France), Samer Abdel Hamid (Clinique Saint Louis, Ganges, France), Laurent Cabaniols, Maxime Robert, Rodolphe Thuret (Centre Hospitalo-Universitaire, H?pital Lapeyronie, Montpellier, France). Pathologists: Drs Didier Brel, Lysiane Schweizer, Philippe Nayraud, C. Lecam-Savin (B?ziers), Roland Daniel, Jean Baptiste Perdigou, Chantal Compan, Mireille Granier, Jean Louis Bouzigues, Elisabeth Broquerie, Jo?lle Simony, Fr?d?ric Bibeau, Pierre Baldet, Isabelle Serre (Montpellier), Marie Laure Gaume (S?te). Biologists: Drs Montels (Service de Biologie M?dicale, Institut du Cancer de Montpellier, Montpellier, France), Dumas (B?ziers, France), Buono (S?te, France), Bonnefille (Lodeve, France), Ruiz (Lunel, France), Paleirac (Clermont-l'H?rault, France). Finally, the authors thank Dr Alexis Elbaz, CESP-INSERM Team Exposome, Heredity, Cancer and Health, for his help on BMI trajectories analyses. The EPICAP study was funded by Ligue nationale contre le cancer, Ligue contre le cancer du Val de Marne, Fondation de France, Agence nationale de s?curit? sanitaire de l'alimentation, de l'environnement et du travail (ANSES). The first author, C?line Lavalette, is funded by a 3-year doctoral allowance from the Paris-Saclay University, for her PhD.
Subjects: 0301 basic medicine, Oncology, Male, Risk, Cancer Research, medicine.medical_specialty, obesity, [SDV]Life Sciences [q-bio], body mass index, Overweight, lcsh:RC254-282, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Internal medicine, Epidemiology, medicine, Humans, Radiology, Nuclear Medicine and imaging, Original Research, Aged, 2. Zero hunger, Prostate cancer risk, business.industry, Incidence, Age Factors, Prostatic Neoplasms, nutritional and metabolic diseases, weight gain, Non-Smokers, Middle Aged, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, prostate cancer, Obesity, 3. Good health, 030104 developmental biology, 030220 oncology & carcinogenesis, Case-Control Studies, trajectory, Life course approach, France, medicine.symptom, business, Body mass index, Weight gain, Cancer Prevention
Abstract: Elevated body mass index (BMI) has been inconsistently associated with prostate cancer occurrence but it has been suggested that life course adulthood obesity may be associated with an increased risk of prostate cancer. However, few studies have investigated lifetime BMI and prostate cancer risk. We analyzed life course BMI trajectories on prostate cancer risk based on data from the Epidemiological study of Prostate Cancer (EPICAP). We included in our analyses 781 incident prostate cancer cases and 829 controls frequency matched by age. Participants were asked about their weight every decade from age 20 to two years before reference date. BMI trajectories were determined using group‐based trajectory modeling to identify groups of men with similar patterns of BMI changes. We identified five BMI trajectories groups. Men with a normal BMI at age 20 developing overweight or obesity during adulthood were at increased risk of aggressive prostate cancer compared to men who maintained a normal BMI. Our results suggest that BMI trajectories resulting in overweight or obesity during adulthood are associated with an increased risk of aggressive prostate cancer, particularly in never smokers, emphasizing the importance of maintaining a healthy BMI throughout adulthood., The influence of body weight during lifetime on PCa risk remains largely ununderstood and has been poorly investigated. Our findings suggest that elevated BMI during adulthood resulting in overweight or obesity is associated with an increased risk of aggressive PCa, emphasizing the importance of maintaining a healthy BMI throughout adulthood.
Published: 2020
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40. Night work and prostate cancer risk: results from the EPICAP Study

Author: Soumaya Ben Khedher, Sylvie Cénée, Xavier Rebillard, Brigitte Trétarre, Pierre-Jean Lamy, Damien Leger, Olivier Cussenot, Méyomo G. Wendeu-Foyet, Geraldine Cancel-Tassin, Virginie Bayon, Brice Faraut, Florence Menegaux, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre du Sommeil et de la Vigilance [Paris], Hôpital Hôtel-Dieu [Paris], Sommeil-Vigilance-Fatigue et Santé Publique (VIFASOM - EA 7330), Université Paris Descartes - Paris 5 (UPD5)-Institut de Recherche Biomédicale des Armées (IRBA), Aide à la Décision pour une Médecine Personnalisé - Laboratoire de Biostatistique, Epidémiologie et Recherche Clinique - EA 2415 (AIDMP), Université Montpellier 1 (UM1)-Université de Montpellier (UM), Centre de Recherche pour les Pathologies Prostatiques (CeRePP), Université Pierre et Marie Curie - Paris 6 (UPMC), Institut universitaire de cancérologie GRC5, Service d'urologie [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Tenon [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de Recherche Biomédicale des Armées (IRBA)-Université Paris Descartes - Paris 5 (UPD5), Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), Institut Universitaire de Cancérologie [Paris] (IUC), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
Subjects: Oncology, Male, Time Factors, Epidemiology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Severity of Illness Index, Shift work, Prostate cancer, 0302 clinical medicine, Risk Factors, Surveys and Questionnaires, Work Schedule Tolerance, Odds Ratio, Medicine, Workplace, Cancer, education.field_of_study, Middle Aged, 030210 environmental & occupational health, Circadian Rhythm, 3. Good health, Occupational Diseases, 030220 oncology & carcinogenesis, 8. Economic growth, Income, France, Employment, medicine.medical_specialty, Evening, Population, [SDV.CAN]Life Sciences [q-bio]/Cancer, 03 medical and health sciences, Occupational Exposure, Internal medicine, Humans, education, Night work, Developing Countries, Aged, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, business.industry, Public Health, Environmental and Occupational Health, Chronotype, Prostatic Neoplasms, medicine.disease, Case-Control Studies, Shift Work, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Neoplasm Grading, Sleep, business
Abstract: ObjectiveTo investigate the role of night work in prostate cancer based on data from the EPICAP Study.MethodsEPICAP is a French population-based case-control study including 818 incident prostate cancer cases and 875 frequency-matched controls that have been interviewed face to face on several potential risk factors including lifetime occupational history. Detailed information on work schedules for each job (permanent or rotating night work, duration, total number of nights, length of the shift, number of consecutive nights) as well as sleep duration and chronotype, was gathered. Prostate cancer aggressiveness was assessed by Gleason Score.ResultsNight work was not associated with prostate cancer, whatever the aggressiveness of prostate cancer, while we observed an overall increased risk among men with an evening chronotype (OR=1.83, 95% CI 1.05 to 3.19). A long duration of at least 20 years of permanent night work was associated with aggressive prostate cancer (OR=1.76, 95% CI 1.13 to 2.75), even more pronounced in combination with a shift length >10 hours or ≥ 6 consecutive nights (OR=4.64, 95% CI 1.78 to 12.13; OR=2.43, 95% CI 1.32 to 4.47, respectively).ConclusionOverall, ever night work, either permanent or rotating, was not associated to prostate cancer. Nevertheless, our results suggest that a long duration of permanent night work in combination with a long shift length or at least six consecutive nights may be associated with prostate cancer, particularly with aggressive prostate cancer. Further studies are needed to confirm those findings.
Published: 2018
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41. Night shift work and breast cancer: a pooled analysis of population-based case–control studies with complete work history

Author: Anne Grundy, Deborah Catherine Glass, John J. Spinelli, Kyriaki Papantoniou, Volker Harth, Pascal Guénel, Manolis Kogevinas, Lin Fritschi, Jane Heyworth, Gemma Castaño-Vinyals, Beate Pesch, Ana Espinosa, Sylvia Rabstein, Kristan J. Aronson, Thomas Brüning, Florence Menegaux, Thomas C. Erren, Emilie Cordina-Duverger, and Alexandru Popa
Subjects: medicine.medical_specialty, Epidemiology, Population, Breast Neoplasms, Risk Assessment, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Work Schedule Tolerance, medicine, Humans, 030212 general & internal medicine, education, education.field_of_study, business.industry, Public health, Absolute risk reduction, Case-control study, Shift Work Schedule, Odds ratio, medicine.disease, Circadian Rhythm, 030220 oncology & carcinogenesis, Cohort, Female, business, Demography
Abstract: Night shift work has been suspected to increase breast cancer risk but epidemiological studies have been inconsistent due to heterogeneous assessment of exposure to night work. To overcome this limitation, we pooled data of five population-based case-control studies from Australia, Canada, France, Germany, and Spain into a single harmonized dataset using a common definition of night work including 6093 breast cancer cases and 6933 population controls. The odds ratio for breast cancer in women who ever worked at night for at least 3 h between midnight and 5 a.m. as compared to never night workers was 1.12 (95% CI 1.00-1.25). Among pre-menopausal women, this odds ratio was 1.26 [1.06-1.51], increasing to 1.36 [1.07-1.74] for night shifts ≥ 10 h, 1.80 [1.20-2.71] for work ≥ 3 nights/week, and 2.55 [1.03-6.30] for both duration of night work ≥ 10 years and exposure intensity ≥ 3 nights/week. Breast cancer risk in pre-menopausal women was higher in current or recent night workers (OR = 1.41 [1.06-1.88]) than in those who had stopped night work more than 2 years ago. Breast cancer in post-menopausal women was not associated with night work whatever the exposure metric. The increase in risk was restricted to ER+ tumors, particularly those who were both ER+ and HER2+ . These results support the hypothesis that night shift work increases the risk of breast cancer in pre-menopausal women, particularly those with high intensity and long duration of exposure. Risk difference between pre- and post-menopausal women deserves further scrutiny.
Published: 2018
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42. Polygenic hazard score is associated with prostate cancer in multi-ethnic populations

Author: Jong Y. Park, Johanna Schleutker, David E. Neal, Karina Dalsgaard Sørensen, Cezary Cybulski, Kay-Tee Khaw, Chun Chieh Fan, Graham G. Giles, Ana Vega, Wesley K. Thompson, Maureen Sanderson, Azad Razack, Florence Menegaux, Chad Huff, Olivier Cussenot, Manolis Kogevinas, Marija Gamulin, Sune F. Nielsen, Nora Pashayan, Lisa F. Newcomb, Maria Elena Martinez, William J. Blot, Hardev Pandha, Ole A. Andreassen, Susan L. Neuhausen, Børge G. Nordestgaard, R. Karunamuni, Catharine M L West, Lorelei A. Mucci, Henrik Grönberg, Catherine M. Tangen, Adam S. Kibel, Jyotsna Batra, Anders M. Dale, Luc Multigner, Barry S. Rosenstein, Stephen Watya, Hermann Brenner, Wei Zheng, Canary Pass Investigators, Rosalind A. Eeles, Robert J. Hamilton, Apcb, Shiv Srivastava, Richard M. Martin, Nc-La PCaP Investigators, Jenny L Donovan, Sonja I. Berndt, Radka Kaneva, Stella Koutros, Freddie C. Hamdy, Yong-Jie Lu, Kim De Ruyck, Jay H. Fowke, Sue A. Ingles, Ian G. Mills, Christiane Maier, Frank Claessens, Kathryn L. Penney, Marie-Élise Parent, Monique J Roobol, Paul A. Townsend, Christopher J. Logothetis, Demetrius Albanes, Stephen N. Thibodeau, Fredrik Wiklund, Manuel R. Teixeira, Nawaid Usmani, Tyler M. Seibert, Jennifer J. Hu, Lisa Cannon-Albright, William S. Bush, Manuela Gago-Dominguez, Robin J Leach, Ruth C. Travis, Eli Marie Grindedal, Zsofia Kote-Jarai, Minh-Phuong Huynh-Le, Alicja Wolk, Esther M. John, Janet L. Stanford, and Kenneth Muir
Subjects: Oncology, 0303 health sciences, medicine.medical_specialty, business.industry, Proportional hazards model, Genetic genealogy, Ethnic group, Distant metastasis, Ethnic populations, medicine.disease, Health equity, 3. Good health, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, 030220 oncology & carcinogenesis, Internal medicine, Genotype, Medicine, business, 030304 developmental biology
Abstract: ObjectivesA polygenic hazard score (PHS1)—weighted sum of 54 single-nucleotide polymorphism genotypes—was previously associated with age at prostate cancer (PCa) diagnosis and improved PCa screening accuracy in Europeans. Performance in more diverse populations is unknown. We evaluated PHS association with PCa in multi-ethnic populations.DesignPHS1 was adapted for compatibility with genotype data from the OncoArray project (PHS2) and tested for association with age at PCa diagnosis, at aggressive PCa diagnosis, and at PCa death.SettingMultiple international institutions.ParticipantsMen with available OncoArray data from the PRACTICAL consortium who were not included in PHS1 development/validation.Main Outcomes and MeasuresPHS2 was tested via Cox proportional hazards models for age at PCa diagnosis, age at aggressive PCa diagnosis (any of: Gleason score ≥7, stage T3-T4, PSA≥10 ng/mL, nodal/distant metastasis), and age at PCa-specific death.Results80,491 men of various self-reported race/ethnicities were included (30,575 controls, 49,916 PCa cases; genetic ancestry groups: 71,856 European, 6,253 African, 2,382 Asian). Median age at last follow-up was 70 years (IQR 63-76); 3,983 PCa deaths, 5,806 other deaths, 70,702 still alive. PHS2 had 46 polymorphisms: 24 directly genotyped and 22 acceptable proxies (r2 ≥0.94). PHS2 was associated with age at PCa diagnosis in the multi-ethnic dataset (z=54, p-16) and in each genetic ancestry group: European (z=56, p-16), Asian (z=47, p-16), African (z=29, p-16). PHS2 was also associated with age at aggressive PCa diagnosis in each genetic ancestry group (p-16) and with age of PCa death in the full dataset (p-16). Comparing the 80th and 20th percentiles of genetic risk, men with high PHS had hazard ratios of 5.3 [95% CI: 5.0-5.7], 5.9 [5.5-6.3], and 5.7 [4.6-7.0] for PCa, aggressive PCa, and PCa-specific death, respectively. Within European, Asian, and African ancestries, analogous hazard ratios for PCa were 5.5 [5.2-5.9], 4.5 [3.2-6.3], and 2.5 [2.1-3.1], respectively.ConclusionsPHS2 is strongly associated with age at PCa diagnosis in a multi-ethnic dataset. PHS2 stratifies men of European, Asian, and African ancestry by genetic risk for any, aggressive, and fatal PCa.Summary boxesWhat is already known on this topicGenetic risk stratification can identify men with greater predisposition for developing prostate cancer, but these risk models may worsen health disparities, as most have only been validated for men of European ancestryA polygenic hazard score was previously associated with age at prostate cancer diagnosis and improved PCa screening accuracy in EuropeansPerformance of the polygenic hazard score in multi-ethnic populations is unknownWhat this study addsIn a dataset from 80,491 men of various self-reported race/ethnicities, the polygenic hazard score was associated with age at prostate cancer diagnosis, aggressive prostate cancer diagnosis, and prostate cancer death.PHS stratifies men of European, Asian, and African ancestry by genetic risk for any, aggressive, and fatal prostate cancer.
Published: 2019
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43. OP110 Body mass index trajectories and prostate cancer risk in the EPICAP study

Author: Pierre-Jean Lamy, Brigitte Trétarre, Florence Menegaux, C Lavalette, E Cordina Duverger, Sylvie Cénée, and Xavier Rebillard
Subjects: education.field_of_study, Cancer prevention, Waist, business.industry, Population, nutritional and metabolic diseases, Odds ratio, Anthropometry, Overweight, medicine, medicine.symptom, Risk factor, education, business, Body mass index, Demography
Abstract: Background High body mass index (BMI) has been inconsistently associated with prostate cancer (PCa) risk. Recent studies suggest that BMI trajectory modeling provides a more robust substitute method to predict cancer risk compared to static measures of BMI. However, only four studies have investigated lifetime BMI and PCa risk. We analyzed the effects of life course BMI trajectories on PCa risk based on data from the Epidemiological study of Prostate Cancer (EPICAP). Methods EPICAP is a French population-based case-control study that enrolled 819 incident cases of PCa diagnosed in 2012 and 2013, aged less than 75 years old and residing in the departement of Herault, France. Controls were 879 age-matched men living in the same geographic area. Face to face interviews, using a standardized computerized questionnaire, gathered information about socio-demographic characteristics, medical history, lifestyle factors, physical activity, residential and occupational history. Anthropometric indicators have been collected through the questionnaire (self-report of height at 18 years old and weight every decades) or anthropometric measures at time of interview (height, weight, waist and hip circumferences). BMI trajectories were determined using group-based trajectory modeling to identify groups of men with similar patterns of BMI change through adulthood. Logistic regression models were used to assess odds ratios (ORs) for the associations between BMI trajectories and PCa risk. Analyses were systematically adjusted for age, family history of PCa and ethnicity. Stratified analyses were conducted by PCa aggressiveness according to the Gleason score. Seeking for relevant interaction between smoking status and BMI trajectories and given that smoking is a major risk factor for many types of cancer, known to decrease obesity, we performed stratified analyses according to smoking status. Results We identified four BMI trajectories groups: ‘stable normal BMI’ (29.7%), ‘normal BMI to overweight’ (50.7%), ‘normal BMI to obesity’ (17.4%) and ‘overweight to obesity’ (2.2%). Men who had a BMI in the normal range at age 20 and developed overweight through adulthood had an increased risk of overall (OR 1.27, [0.99–1.62]) and aggressive (OR 1.57, [1.03–2.39]) PCa risk compared to men who maintained a normal BMI. Increased risk of aggressive PCa was also observed among never smokers who developed overweight (OR 3.32, [1.29–8.53]) or obesity (OR 4.19, [1.30–13.51]), but interaction was not significant. Conclusion Our results suggest that BMI trajectories resulting in overweight or obesity during adulthood are associated with an increased risk of PCa, emphasizing the importance of maintaining a normal BMI throughout adulthood for cancer prevention.
Published: 2019
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44. P31 Abdominal obesity and prostate cancer risk: results from the EPICAP study

Author: E Cordina Duverger, Xavier Rebillard, Brigitte Trétarre, Pierre-Jean Lamy, Sylvie Cénée, C Lavalette, and Florence Menegaux
Subjects: education.field_of_study, Waist, business.industry, Population, Odds ratio, Anthropometry, medicine, Family history, Risk factor, medicine.symptom, business, education, Body mass index, Abdominal obesity, Demography
Abstract: Background Obesity is associated with an increased risk of several cancers, but the relationship between obesity and prostate cancer (PCa) remains controversial. We showed than body mass index (BMI) itself is not associated with PCa, while central obesity indicators, such as waist circumference (WC) or waist-hip ratio (WHR), were associated with increased risks of PCa. To further explore this relationship and given the accumulating evidence between BMI and smoking in cancer risk, we conducted further analyses taking into account smoking status within the EPICAP study. Methods EPICAP is a French population-based case-control study that enrolled 819 incident cases of PCa diagnosed in 2012 and 2013, aged less than 75 years old and residing in the departement of Herault, France. Controls were 879 age-matched individuals living in the same geographic area. Face to face interviews, using a standardized computerized questionnaire, gathered information about socio-demographic characteristics, personal medical history, lifestyle factors, physical activity, residential and occupational history. Anthropometric indicators have also been collected through the questionnaire (self-report of height at 18 years old and weight every decades) or anthropometric measures at time of interview (height, weight, waist and hip circumferences). Logistic regression models were used to assess odds ratios (ORs) for the associations between anthropometric indicators (BMI, WC, WHR) and PCa risk. Analyses were adjusted for age, family history of PCa and ethnicity. Stratified analyses were conducted by PCa aggressiveness according to the Gleason score. Seeking for relevant interaction between smoking status and BMI trajectories and given that smoking is a major risk factor for many types of cancer, known to decrease obesity, we performed stratified analyses according to smoking status. Results Overall, 28.6% were never smokers, 54.9% former smokers, and 16.5% current smokers, similarly distributed between cases and controls (p=0.21). Among never smokers, we observed a slight but not significant increased risk of overall PCa for men with a BMI above 25 kg/m2; (OR 1.52 [0.97–2.38]) as well as for men with a WC greater to 94 cm (OR 1.42 [0.93–2.16]) or a WHR greater or equal to 0.95 (OR 1.40 [0.92–2.13]). Among current smokers, we observed no association between BMI, WC or WHR and PCa risk (OR 1.15 [0.62–2.13], OR 1.24 [0.68–2.30], OR 1.06 [0.58–1.93], respectively). However interaction was not significant. Conclusion Our results showed that associations between anthropometric indicators were more pronounced among never smokers, in agreement with the assumption that smoking may attenuate the association between obesity and cancer.
Published: 2019
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45. Author Correction: Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci

Author: Robert J. Hamilton, Douglas F. Easton, Suzanne K. Chambers, Edward Giovannucci, Henrik Grönberg, Artitaya Lophatananon, Niclas Håkansson, Sue A. Ingles, Markus Aly, Antonio Gómez-Caamaño, B. E. Henderson, Samantha E.T. Larkin, Manuel Luedeke, Fredrick R. Schumacher, Zan Sun, Karina Dalsgaard Sørensen, Jasmine Lim, Marija Gamulin, Lu Y-J., Meir J. Stampfer, Shannon K. McDonnell, Maria Elena Martinez, Harry Ostrer, Piet Ost, Michael Borre, Monique J. Roobol, F Canzian, D J Schaid, Lin H-Y., Rasmus Bisbjerg, Judith A. Clements, Ezequiel Anokian, Martin Andreas Røder, Ed Saunders, Agnieszka Michael, G Jenster, Bernd Holleczek, Guomin Wang, Jakub Lubiński, Jeri Kim, Genetic Associations, Rosalind A. Eeles, Yves Akoli Koudou, Gemma Castaño-Vinyals, Jing Ma, Leire Moya, Sonja I. Berndt, Thérèse Truong, Maren Weischer, Robert Szulkin, T. Van Den Broeck, Davor Lessel, Børge G. Nordestgaard, Chee Goh, Torben F. Ørntoft, Manolis Kogevinas, Catherine M. Tangen, Gerald L. Andriole, Robert N. Hoover, Ana Vega, Stephanie J. Weinstein, West Cml., Tomislav Kuliš, Neil Fleshner, Graham G. Giles, Barry S. Rosenstein, Z Cui, Marta Cardoso, Tokhir Dadaev, Jenny L Donovan, David E. Neal, Richard M. Martin, Tyrer Jp, Thomas J. Schnoeller, Sandeep Singhal, Clara Cieza-Borrella, Ian M. Thompson, Lisa A. Cannon-Albright, Jong Y. Park, Johanna Schleutker, Brian D. Carter, Esther M. John, Christiane Maier, Matthew Parliament, Antonio Finelli, Mark N. Brook, Gail P. Risbridger, Xin Guo, Lisa G. Horvath, Daniel W. Lin, Mariana C. Stern, Tobias Nordström, Demetrius Albanes, Melissa C. Southey, Zhang H-W., Liesel M. FitzGerald, Christopher I. Amos, Freddie C. Hamdy, P Pharoah, Wayne D. Tilley, Susan M. Gapstur, Teo S-H., Claire Aukim-Hastie, Christopher J. Logothetis, Elio Riboli, Bettina F. Drake, Csilla Sipeky, Alicja Wolk, Cezary Cybulski, Joe Dennis, Olama Aaa., Hermann Brenner, Lorelei A. Mucci, Yuan Chun Ding, L E Beane Freeman, Stella Koutros, G De Meerleer, A. Siddiq, Lisa F. Newcomb, Mitchell J. Machiela, Munaza Ahmed, Jyotsna Batra, Susan L. Neuhausen, Christopher A. Haiman, Stephen J. Chanock, T A Sellers, Florence Menegaux, David V. Conti, Lovise Maehle, O. Cussenot, Neil G. Burnet, Nora Pashayan, Timothy J. Key, P Iversen, Hardev Pandha, Katarina Cuk, David J. Hunter, Khaw K-T., Janet L. Stanford, Loic Le Marchand, Javier Llorca, Steven Joniau, Elaine A. Ostrander, Sarah L. Kerns, van Schaik Rhn., Adam S. Kibel, Robert J. MacInnis, Tammela Tlj., Sune F. Nielsen, Constance Turman, Peter Kraft, Laurence N. Kolonel, Nawaid Usmani, K. De Ruyck, Sara Benlloch, C. Slavov, Azad Hassan Abdul Razack, Milan S. Geybels, Jianfeng Xu, Phyllis J. Goodman, Martin Eklund, Alison M. Dunning, Radka Kaneva, Paul A. Townsend, Kenneth Muir, Manuel R. Teixeira, Sara Lindström, Geraldine Cancel-Tassin, Mechanisms in Oncology, Anssi Auvinen, Victoria L. Stevens, Laura Fachal, Stephen N. Thibodeau, Linda Steele, Manuela Gago-Dominguez, Frank Claessens, Kathryn L. Penney, Fredrik Wiklund, Eli Marie Grindedal, Xin Sheng, Ruth C. Travis, Zsofia Kote-Jarai, Dominika Wokołorczyk, D. Leongamornlert, Paula Paulo, Xueying Mao, Vanio Mitev, Jose Esteban Castelao, and Ninghan Feng
Subjects: Oncology, 0303 health sciences, medicine.medical_specialty, Published Erratum, MEDLINE, Impact study, PROSTATE CANCER SUSCEPTIBILITY, Biology, urologic and male genital diseases, Article, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Genetics, medicine, Association (psychology), Biological sciences, 030217 neurology & neurosurgery, 030304 developmental biology
Abstract: Genome-wide association studies (GWAS) and fine-mapping efforts to date have identified more than 100 prostate cancer (PrCa)-susceptibility loci. We meta-analyzed genotype data from a custom high-density array of 46,939 PrCa cases and 27,910 controls of European ancestry with previously genotyped data of 32,255 PrCa cases and 33,202 controls of European ancestry. Our analysis identified 62 novel loci associated (PC, p.Pro1054Arg) in ATM and rs2066827 (OR = 1.06; P = 2.3 × 10(−9); T>G, p.Val109Gly) in CDKN1B. The combination of all loci captured 28.4% of the PrCa familial relative risk, and a polygenic risk score conferred an elevated PrCa risk for men in the ninetieth to ninety-ninth percentiles (relative risk = 2.69; 95% confidence interval (CI): 2.55–2.82) and first percentile (relative risk = 5.71; 95% CI: 5.04–6.48) risk stratum compared with the population average. These findings improve risk prediction, enhance fine-mapping, and provide insight into the underlying biology of PrCa(1).
Published: 2019

46. Author Correction: Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Author: Annette Juul Vangsted, van, Duin, M, David E. Neal, Peter Hoffmann, A Wolk, Robert J. Hamilton, Anthony J. Swerdlow, F. Wiklund, De, Ruyck, K, Paul A. Townsend, S. N. Thibodeau, Asta Försti, Esther M. John, Unnur Thorsteinsdottir, W Gregory, Niels Frost Andersen, Peter Broderick, A-K Wihlborg, Frank Claessens, Doug Easton, Kathryn L. Penney, Keith W. Muir, Jeri Kim, Jonathan S. Mitchell, Johanna Schleutker, G Cancel-Tassin, Barry S. Rosenstein, Jy Park, Hauke Thomsen, Rowan Kuiper, C West, H Gronberg, Mina Ali, CM Tangen, Obul Reddy Bandapalli, Ana Vega, Faith E. Davies, Rosalind A. Eeles, Daniel F. Gudbjartsson, Fredrick R. Schumacher, Janet L. Stanford, Paul D.P. Pharoah, Owen W. Stephens, Monique J. Roobol, Richard S. Houlston, Gudmar Thorleifsson, Christian Langer, Susan L. Neuhausen, S Chanock, G.G. Giles, Azad Razack, S Koutros, F Canzian, S Benlloch, H. Einsele, Kari Hemminki, KD Sorensen, Y-J Lu, K-T Khaw, Hareth Nahi, FC Hamdy, D Albanes, Christopher A. Haiman, Ellinor Johnsson, Amit Sud, Adam S. Kibel, Pieter Sonneveld, Florence Menegaux, Manolis Kogevinas, Nawaid Usmani, Annemiek Broyl, K. H. Jöckel, Jolanta Nickel, David W. Johnson, Aaa Olama, B.G. Nordestgaard, Amy Holroyd, Niels Weinhold, Cezary Cybulski, Sigurdur Y. Kristinsson, Radka Kaneva, Ruth C. Travis, Kari Stefansson, SI Berndt, Bowang Chen, Scott Kimber, Davor Lessel, Philip J. Law, M. M. Nöthen, Lisa A. Cannon-Albright, BE Henderson, Ni Li, Urban Gullberg, Uta Bertsch, S Weinstein, Nora Pashayan, Christiane Maier, H Brenner, Ingemar Turesson, Hardev Pandha, Thorunn Rafnar, Alison M. Dunning, Fiona M. Ross, Graham Jackson, David V. Conti, Sue A. Ingles, da, Silva, Filho, Mi, Jens Hillengass, Lisa F. Newcomb, Giulia Orlando, Brian A Walker, Teixeira, Björn Nilsson, Jenny L Donovan, Molly Went, U. H. Mellqvist, Chiara Campo, Zsofia Kote-Jarai, VL Stevens, Martin Kaiser, B-M Halvarsson, J Clements, Martin Hansson, Manuela Gago-Dominguez, EM Grindedal, Anders Waage, Julian Peto, L Mucci, Gareth J. Morgan, J Batra, and H. Goldschmidt
Subjects: Male, Quality Control, Risk, 0301 basic medicine, Chromatin Immunoprecipitation, Genotype, Computer science, Science, Quantitative Trait Loci, Medizin, General Physics and Astronomy, Genome-wide association study, 02 engineering and technology, computer.software_genre, Polymorphism, Single Nucleotide, White People, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Humans, Genetic Predisposition to Disease, lcsh:Science, Author Correction, Promoter Regions, Genetic, Multidisciplinary, business.industry, Bayes Theorem, General Chemistry, 021001 nanoscience & nanotechnology, Chromatin, Spelling, Identification (information), 030104 developmental biology, Gene Expression Regulation, Cancer genetics, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, lcsh:Q, Female, Artificial intelligence, Multiple Myeloma, 0210 nano-technology, business, computer, Natural language processing, Genome-Wide Association Study
Abstract: Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight into the biological basis of MM.
Published: 2019
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47. Estimation of breast, prostate, and colorectal cancer incidence using a French administrative database (general sample of health insurance beneficiaries)

Author: S. Doat, Anne Fagot-Campagna, Florence Menegaux, S. Samson, and Philippe Tuppin
Subjects: Adult, Male, medicine.medical_specialty, Databases, Factual, Epidemiology, Colorectal cancer, Breast Neoplasms, 030501 epidemiology, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Breast cancer, Internal medicine, medicine, Humans, Registries, 030212 general & internal medicine, Reimbursement, Aged, Gynecology, business.industry, Incidence, Insurance Benefits, Incidence (epidemiology), Public Health, Environmental and Occupational Health, Prostatic Neoplasms, Middle Aged, medicine.disease, Cancer registry, Hospitalization, Standardized mortality ratio, Cohort, Female, France, Colorectal Neoplasms, 0305 other medical science, business
Abstract: Aim The aim of this study was to compare incidence of breast, prostate, and colorectal cancer incidence estimated from a French administrative database with the incidences estimated from the cancer registry data. Materials and methods A cohort of 426,410 people included in the general sample of health insurance beneficiaries (EGB) database as of January 1, 2007, was constituted. Several algorithms were developed to estimate cancer incidence between 2008 and 2012 using principal diagnosis (PD) of hospital discharge data (medical information systems program [PMSI]) and/or long-term disease (LTD) and together with a procedure necessary for histological diagnosis and indicating initial disease management. The incidence rates obtained were compared with those from the registry data using the standardized incidence ratio (SIR). Results The algorithm taking into account LTD and PD in the PMSI and the mandatory presence of a marker procedure provided estimates close to those from the registry data for breast cancer (SIR: 1.12 [1.07–1.18]) and colorectal cancer (SIR: 0.94 [0.88–1.02] in men and SIR: 0.93 [0.86–1.01] in women). For prostate cancer, taking into account specific procedures and drugs in addition to LTD and PD in the PMSI enhanced the estimation of incidence (SIR: 1.03 [0.98–1.08]). Conclusion The PMSI together with reimbursement data (LTD, procedures, drugs) provided estimates of breast, prostate, and colorectal cancer incidence, at a national level, comparable to those from the cancer registry data.
Published: 2016
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48. Abstract 3517: A germline variant at 8q24 contributes to familial clustering of prostate cancer in men of African ancestry

Author: Victoria L. Stevens, Graham Casey, Rick A. Kittles, Geraldine Cancel-Tassin, Rosalind A. Eeles, Jong Y. Park, Marie-Élise Parent, Jianfeng Xu, Shiv Srivastava, James L. Mohler, Jack A. Taylor, Esther M. John, Sonja I. Berndt, William J. Blot, Stephen J. Chanock, Christopher A. Haiman, Florence Menegaux, Gary J. Smith, Barbara Nemesure, Janet L. Stanford, Jay H. Fowke, Wei Zheng, Benjamin A. Rybicki, Phyllis J. Goodman, Adam S. Kibel, Thomas A. Sellers, Eric A. Klein, Anselm Hennis, Dana C. Crawford, Maureen Sanderson, Olivier Cussenot, Elizabeth T. H. Fontham, William B. Isaacs, Jennifer Cullen, John D. Carpten, Robin J. Leach, Diptasri Mandal, Sue A. Ingles, Burcu F. Darst, Luc Multigner, Laurent Brureau, David V. Conti, Stephen Watya, Ian M. Thompson, Zsofia Kote-Jarai, Jennifer J. Hu, Kathleen A. Cooney, Elaine A. Ostrander, Chad D. Huff, and Jeannette T. Bensen
Subjects: Cancer Research, education.field_of_study, business.industry, Population, Cancer, Familial clustering, Genome-wide association study, medicine.disease, Germline, Prostate cancer, Oncology, Medicine, Family history, Risk factor, education, business, Demography
Abstract: Germline variation at 8q24 is the strongest risk factor for prostate cancer (PCa) across all racial and ethnic populations. While most 8q24 associations have been observed across populations, rs72725854 [T risk allele frequency ~6%] is only found in men of African ancestry and is the strongest known genome-wide association signal for PCa in this population. We investigated whether the T allele of rs72725854 is associated with PCa family history and age at diagnosis, characteristics known to have a strong genetic component. Analyses were performed using a sample of 9,052 cases and 8,595 controls from the African Ancestry Prostate Cancer (AAPC) GWAS Consortium and the ELLIPSE/PRACTICAL OncoArray Consortium. Participants were unselected for PCa family history. Among cases, 23.7% carried at least one copy of the T allele versus 11.6% of controls. The OR was 2.29 (95% CI=2.10–2.49) for TA heterozygotes and 5.04 (95% CI=3.36–7.55) for TT homozygotes. The percentage of cases carrying the T allele was significantly greater for men with a PCa family history (27.4% vs. 22.7% without a family history, p=0.002) and for men diagnosed 100 ng/ml or death from PCa), 25.4% for high-risk disease (stage T3/T4, Gleason 8-10, or PSA=20-100 ng/ml), 24.6% for intermediate-risk disease (Gleason=7, stage T1/T2, and PSA=10-20 ng/ml), and 21.4% for low-risk disease (Gleason Citation Format: Burcu F. Darst, Jeannette T. Bensen, Sue A. Ingles, Benjamin A. Rybicki, Barbara Nemesure, Esther M. John, Jay H. Fowke, Victoria L. Stevens, Sonja I. Berndt, Chad D. Huff, Jong Y. Park, Wei Zheng, Elaine A. Ostrander, Shiv Srivastava, John Carpten, Thomas A. Sellers, Maureen Sanderson, Dana C. Crawford, Olivier Cussenot, Jennifer Cullen, Rick A. Kittles, Jianfeng Xu, Zsofia Kote-Jarai, Luc Multigner, Marie-Elise Parent, Florence Menegaux, Geraldine Cancel-Tassin, Adam S. Kibel, Eric A. Klein, Phyllis J. Goodman, Jennifer J. Hu, Graham Casey, Anselm J. Hennis, Ian M. Thompson, Robin Leach, James L. Mohler, Elizabeth T. Fontham, Gary J. Smith, Jack A. Taylor, Rosalind A. Eeles, Laurent Brureau, Stephen J. Chanock, Stephen Watya, Janet L. Stanford, Diptasri Mandal, William B. Isaacs, Kathleen A. Cooney, William J. Blot, David V. Conti, Christopher A. Haiman. A germline variant at 8q24 contributes to familial clustering of prostate cancer in men of African ancestry [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 3517.
Published: 2020
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49. Circadian genes and risk of prostate cancer: Findings from the EPICAP study

Author: Méyomo G, Wendeu-Foyet, Yves, Koudou, Sylvie, Cénée, Brigitte, Trétarre, Xavier, Rébillard, Géraldine, Cancel-Tassin, Olivier, Cussenot, Anne, Boland, Delphine, Bacq, Jean-François, Deleuze, Pierre-Jean, Lamy, Claire, Mulot, Pierre, Laurent-Puig, Thérèse, Truong, and Florence, Menegaux
Subjects: Adult, Male, Prostatic Neoplasms, Nerve Tissue Proteins, Nuclear Receptor Subfamily 1, Group F, Member 1, Period Circadian Proteins, Middle Aged, Case-Control Studies, Circadian Clocks, Basic Helix-Loop-Helix Transcription Factors, Odds Ratio, Humans, Gene Regulatory Networks, Genetic Predisposition to Disease, Neoplasm Grading, Genetic Association Studies, Aged
Abstract: Circadian rhythms regulate several physiological functions and genes controlling the circadian rhythm were found to regulate cell proliferation, cell cycle and apoptosis. Few studies have investigated the role of those circadian genes in prostate cancer occurrence. We aim to investigate the relationship between circadian genes polymorphisms and prostate cancer risk based on data from the EPICAP study, a population-based case-control study including 1,515 men (732 cases / 783 controls) with genotyped data. Odds Ratios (ORs) for association between prostate cancer and circadian gene variants were estimated for each of the 872 single nucleotide polymorphisms (SNPs) in 31 circadian clock genes. We also used a gene-based and pathway-based approach with a focus on the pathway including 9 core circadian genes. Separate analyses were conducted by prostate cancer aggressiveness. The core-circadian pathway (p = 0.0006) was significantly associated to prostate cancer, for either low (p = 0.002) or high (p = 0.01) grade tumor. At the gene level, we observed significant associations between all prostate cancer and NPAS2 and PER1 after correcting for multiple testing, while only RORA was significant for aggressive tumors. At the SNP-level, no significant association was observed. Our findings provide additional evidence of a potential link between genetic variants in circadian genes and prostate cancer risk. Further investigation is warranted to confirm these findings and to better understand the biological pathways involved.
Published: 2018

50. Publisher Correction: Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation

Author: Maya Ghoussaini, Stacey L. Edwards, Kyriaki Michailidou, Silje Nord, Richard Cowper-Sal·lari, Kinjal Desai, Siddhartha Kar, Kristine M. Hillman, Susanne Kaufmann, Dylan M. Glubb, Jonathan Beesley, Joe Dennis, Manjeet K. Bolla, Qin Wang, Ed Dicks, Qi Guo, Marjanka K. Schmidt, Mitul Shah, Robert Luben, Judith Brown, Kamila Czene, Hatef Darabi, Mikael Eriksson, Daniel Klevebring, Stig E. Bojesen, Børge G. Nordestgaard, Sune F. Nielsen, Henrik Flyger, Diether Lambrechts, Bernard Thienpont, Patrick Neven, Hans Wildiers, Annegien Broeks, Laura J. Van’t Veer, Emiel J. Th Rutgers, Fergus J. Couch, Janet E. Olson, Emily Hallberg, Celine Vachon, Jenny Chang-Claude, Anja Rudolph, Petra Seibold, Dieter Flesch-Janys, Julian Peto, Isabel dos-Santos-Silva, Lorna Gibson, Heli Nevanlinna, Taru A. Muranen, Kristiina Aittomäki, Carl Blomqvist, Per Hall, Jingmei Li, Jianjun Liu, Keith Humphreys, Daehee Kang, Ji-Yeob Choi, Sue K. Park, Dong-Young Noh, Keitaro Matsuo, Hidemi Ito, Hiroji Iwata, Yasushi Yatabe, Pascal Guénel, Thérèse Truong, Florence Menegaux, Marie Sanchez, Barbara Burwinkel, Frederik Marme, Andreas Schneeweiss, Christof Sohn, Anna H. Wu, Chiu-chen Tseng, David Van Den Berg, Daniel O. Stram, Javier Benitez, M Pilar Zamora, Jose Ignacio Arias Perez, Primitiva Menéndez, Xiao-Ou Shu, Wei Lu, Yu-Tang Gao, Qiuyin Cai, Angela Cox, Simon S. Cross, Malcolm W. R. Reed, Irene L. Andrulis, Julia A. Knight, Gord Glendon, Sandrine Tchatchou, Elinor J. Sawyer, Ian Tomlinson, Michael J. Kerin, Nicola Miller, Christopher A. Haiman, Brian E. Henderson, Fredrick Schumacher, Loic Le Marchand, Annika Lindblom, Sara Margolin, Soo Hwang Teo, Cheng Har Yip, Daphne S. C. Lee, Tien Y. Wong, Maartje J. Hooning, John W. M. Martens, J. Margriet Collée, Carolien H. M. van Deurzen, John L. Hopper, Melissa C. Southey, Helen Tsimiklis, Miroslav K. Kapuscinski, Chen-Yang Shen, Pei-Ei Wu, Jyh-Cherng Yu, Shou-Tung Chen, Grethe Grenaker Alnæs, Anne-Lise Borresen-Dale, Graham G. Giles, Roger L. Milne, Catriona McLean, Kenneth Muir, Artitaya Lophatananon, Sarah Stewart-Brown, Pornthep Siriwanarangsan, Mikael Hartman, Hui Miao, Shaik Ahmad Bin Syed Buhari, Yik Ying Teo, Peter A. Fasching, Lothar Haeberle, Arif B. Ekici, Matthias W. Beckmann, Hermann Brenner, Aida Karina Dieffenbach, Volker Arndt, Christa Stegmaier, Anthony Swerdlow, Alan Ashworth, Nick Orr, Minouk J. Schoemaker, Montserrat García-Closas, Jonine Figueroa, Stephen J. Chanock, Jolanta Lissowska, Jacques Simard, Mark S. Goldberg, France Labrèche, Martine Dumont, Robert Winqvist, Katri Pylkäs, Arja Jukkola-Vuorinen, Hiltrud Brauch, Thomas Brüning, Yon-Dschun Koto, Paolo Radice, Paolo Peterlongo, Bernardo Bonanni, Sara Volorio, Thilo Dörk, Natalia V. Bogdanova, Sonja Helbig, Arto Mannermaa, Vesa Kataja, Veli-Matti Kosma, Jaana M. Hartikainen, Peter Devilee, Robert A. E. M. Tollenaar, Caroline Seynaeve, Christi J. Van Asperen, Anna Jakubowska, Jan Lubinski, Katarzyna Jaworska-Bieniek, Katarzyna Durda, Susan Slager, Amanda E. Toland, Christine B. Ambrosone, Drakoulis Yannoukakos, Suleeporn Sangrajrang, Valerie Gaborieau, Paul Brennan, James McKay, Ute Hamann, Diana Torres, Wei Zheng, Jirong Long, Hoda Anton-Culver, Susan L. Neuhausen, Craig Luccarini, Caroline Baynes, Shahana Ahmed, Mel Maranian, Catherine S. Healey, Anna González-Neira, Guillermo Pita, M Rosario Alonso, Nuria Álvarez, Daniel Herrero, Daniel C. Tessier, Daniel Vincent, Francois Bacot, Ines de Santiago, Jason Carroll, Carlos Caldas, Melissa A. Brown, Mathieu Lupien, Vessela N. Kristensen, Paul D. P. Pharoah, Georgia Chenevix-Trench, Juliet D. French, Douglas F. Easton, and Alison M. Dunning
Subjects: Oncology, medicine.medical_specialty, Multidisciplinary, business.industry, Published Erratum, MEDLINE, General Physics and Astronomy, Locus (genetics), General Chemistry, medicine.disease, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, 030220 oncology & carcinogenesis, Internal medicine, medicine, 030212 general & internal medicine, business
Abstract: GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the ‘iCOGS’ genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against >100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84−0.87; P=1.7 × 10−43) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology., Previous studies identified an association between the 2q35 locus and breast cancer. Here, the authors show that a SNP at 2q35, rs4442975, is associated with oestrogen receptor positive disease and suggest that this effect is mediated through the downregulation of a known breast cancer gene, IGFBP5.
Published: 2018

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