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55 results on '"Kluźniak, Wojciech"'

51. Do BARD1 Mutations Confer an Elevated Risk of Prostate Cancer?

Author

Stempa, Klaudia, Wokołorczyk, Dominika, Kluźniak, Wojciech, Rogoża-Janiszewska, Emilia, Malińska, Karolina, Rudnicka, Helena, Huzarski, Tomasz, Gronwald, Jacek, Gliniewicz, Katarzyna, Dębniak, Tadeusz, Jakubowska, Anna, Lener, Marcin, Tomiczek-Szwiec, Joanna, Domagała, Paweł, Suszynska, Malwina, Kozlowski, Piotr, Kluz, Tomasz, Naczk, Mariusz, Lubiński, Jan, and Narod, Steven A.

Subjects
GENETIC mutation, CONFIDENCE intervals, BRCA genes, MEDICAL screening, CANCER patients, DISEASE susceptibility, DESCRIPTIVE statistics, DISEASE prevalence, ODDS ratio, PROSTATE tumors, DISEASE risk factors
Abstract

Simple Summary: Current cancer testing gene panels tend to be comprehensive. One of the genes commonly included in the testing panels is BARD1. To establish whether BARD1 mutations predispose to prostate cancer, we sequenced BARD1 in 390 hereditary prostate cancer cases, genotyped 5715 men with unselected prostate cancer and 10,252 controls for three recurrent rare BARD1 variants in Poland. We did not see an elevated prostate risk cancer given p.Q564X truncating mutation, p.R658C missense mutation and p.R659= synonymous variant. Neither variant influenced prostate cancer characteristics or survival. Our study is the first to evaluate the association between BARD1 mutations and prostate cancer susceptibility. It is not justified to inform men about increased prostate cancer risk in case of identification of a BARD1 mutation. However, a female relative of a man with a BARD1 mutation may benefit from this information and be tested, because BARD1 is a breast cancer susceptibility gene. The current cancer testing gene panels tend to be comprehensive rather than site-specific. BARD1 is one of the genes commonly included in the multi-cancer testing panels. Mutations in BARD1 confer an increase in the risk for breast cancer, but it is not studied whether or not they predispose to prostate cancer. To establish if BARD1 mutations also predispose to prostate cancer, we screened BARD1 in 390 Polish patients with hereditary prostate cancer. No truncating mutations were identified by sequencing. We also genotyped 5715 men with unselected prostate cancer, and 10,252 controls for three recurrent BARD1 variants, including p.Q564X, p.R658C and p.R659=. Neither variant conferred elevated risk of prostate cancer (ORs between 0.84 and 1.15, p-values between 0.57 and 0.93) nor did they influence prostate cancer characteristics or survival. We conclude that men with a BARD1 mutation are not at elevated prostate cancer risk. It is not justified to inform men about increased prostate cancer risk in case of identification of a BARD1 mutation. However, a female relative of a man with a BARD1 mutation may benefit from this information and be tested for the mutation, because BARD1 is a breast cancer susceptibility gene. [ABSTRACT FROM AUTHOR]

Published
2021
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52. A meta-analysis of 87,040 individuals identifies 23 new susceptibility loci for prostate cancer

Author

Al Olama, Ali Amin, Kote-Jarai, Zsofia, Berndt, Sonja I., Conti, David V., Schumacher, Fredrick, Han, Ying, Benlloch, Sara, Hazelett, Dennis J., Wang, Zhaoming, Saunders, Ed, Leongamornlert, Daniel, Lindstrom, Sara, Jugurnauth-Little, Sara, Dadaev, Tokhir, Tymrakiewicz, Malgorzata, Stram, Daniel O., Rand, Kristin, Wan, Peggy, Stram, Alex, Sheng, Xin, Pooler, Loreall C., Park, Karen, Xia, Lucy, Tyrer, Jonathan, Kolonel, Laurence N., Le Marchand, Loic, Hoover, Robert N., Machiela, Mitchell J., Yeager, Merideth, Burdette, Laurie, Chung, Charles C., Hutchinson, Amy, Yu, Kai, Goh, Chee, Ahmed, Mahbubl, Govindasami, Koveela, Guy, Michelle, Tammela, Teuvo L.J., Auvinen, Anssi, Wahlfors, Tiina, Schleutker, Johanna, Visakorpi, Tapio, Leinonen, Katri A., Xu, Jianfeng, Aly, Markus, Donovan, Jenny, Travis, Ruth C., Key, Tim J., Siddiq, Afshan, Canzian, Federico, Khaw, Kay-Tee, Takahashi, Atsushi, Kubo, Michiaki, Pharoah, Paul, Pashayan, Nora, Weischer, Maren, Nordestgaard, Borge G., Nielsen, Sune F., Klarskov, Peter, Røder, Martin Andreas, Iversen, Peter, Thibodeau, Stephen N., McDonnell, Shannon K, Schaid, Daniel J, Stanford, Janet L., Kolb, Suzanne, Holt, Sarah, Knudsen, Beatrice, Coll, Antonio Hurtado, Gapstur, Susan M., Diver, W. Ryan, Stevens, Victoria L., Maier, Christiane, Luedeke, Manuel, Herkommer, Kathleen, Rinckleb, Antje E., Strom, Sara S., Pettaway, Curtis, Yeboah, Edward D., Tettey, Yao, Biritwum, Richard B., Adjei, Andrew A., Tay, Evelyn, Truelove, Ann, Niwa, Shelley, Chokkalingam, Anand P., Cannon-Albright, Lisa, Cybulski, Cezary, Wokołorczyk, Dominika, Kluźniak, Wojciech, Park, Jong, Sellers, Thomas, Lin, Hui-Yi, Isaacs, William B., Partin, Alan W., Brenner, Hermann, Dieffenbach, Aida Karina, Stegmaier, Christa, Chen, Constance, Giovannucci, Edward L., Ma, Jing, Stampfer, Meir, Penney, Kathryn L., Mucci, Lorelei, John, Esther M., Ingles, Sue A., Kittles, Rick A., Murphy, Adam B., Pandha, Hardev, Michael, Agnieszka, Kierzek, Andrzej M., Blot, William, Signorello, Lisa B., Zheng, Wei, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Nemesure, Barbara, Carpten, John, Leske, Cristina, Wu, Suh-Yuh, Hennis, Anselm, Kibel, Adam S., Rybicki, Benjamin A., Neslund-Dudas, Christine, Hsing, Ann W., Chu, Lisa, Goodman, Phyllis J., Klein, Eric A, Zheng, S. Lilly, Batra, Jyotsna, Clements, Judith, Spurdle, Amanda, Teixeira, Manuel R., Paulo, Paula, Maia, Sofia, Slavov, Chavdar, Kaneva, Radka, Mitev, Vanio, Witte, John S., Casey, Graham, Gillanders, Elizabeth M., Seminara, Daniella, Riboli, Elio, Hamdy, Freddie C., Coetzee, Gerhard A., Li, Qiyuan, Freedman, Matthew L., Hunter, David J., Muir, Kenneth, Gronberg, Henrik, Neal, David E., Southey, Melissa, Giles, Graham G., Severi, Gianluca, Cook, Michael B., Nakagawa, Hidewaki, Wiklund, Fredrik, Kraft, Peter, Chanock, Stephen J., Henderson, Brian E., Easton, Douglas F., Eeles, Rosalind A., and Haiman, Christopher A.

Abstract

Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of >10 million SNPs in 43,303prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three novel susceptibility loci were revealed at P<5×10-8; 15 variants were identified among men of European ancestry, 7 from multiethnic analyses and one was associated with early-onset prostate cancer. These 23 variants, in combination with the known prostate cancer risk variants, explain 33% of the familial risk of the disease in European ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the utility of combining ancestrally diverse populations to discover risk loci for disease.

Published
2014
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53. Corrigendum: Germline RECQL mutations are associated with breast cancer susceptibility

Author

Cybulski, Cezary, Carrot-Zhang, Jian, Kluźniak, Wojciech, Rivera, Barbara, Kashyap, Aniruddh, Wokołorczyk, Dominika, Giroux, Sylvie, Nadaf, Javad, Hamel, Nancy, Zhang, Shiyu, Huzarski, Tomasz, Gronwald, Jacek, Byrski, Tomasz, Szwiec, Marek, Jakubowska, Anna, Rudnicka, Helena, Lener, Marcin, Masojć, Bartłomiej, Tonin, Patrica N, Rousseau, Francois, Górski, Bohdan, Dębniak, Tadeusz, Majewski, Jacek, Lubiński, Jan, Foulkes, William D, Narod, Steven A, and Akbari, Mohammad R

Published
2016
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54. Polygenic hazard score to guide screening for aggressive prostate cancer : development and validation in large scale cohorts

Author

The PRACTICAL Consortium, Seibert, Tyler M, Fan, Chun Chieh, Wang, Yunpeng, Zuber, Verena, Karunamuni, Roshan, Parsons, J Kellogg, Eeles, Rosalind A, Easton, Douglas F, Kote-Jarai, ZSofia, Olama, Ali Amin Al, Garcia, Sara Benlloch, Muir, Kenneth, Grönberg, Henrik, Wiklund, Fredrik, Aly, Markus, Schleutker, Johanna, Sipeky, Csilla, Tammela, Teuvo LJ, Nordestgaard, Børge G, Nielsen, Sune F, Weischer, Maren, Bisbjerg, Rasmus, Røder, M Andreas, Iversen, Peter, Key, Tim J, Travis, Ruth C, Neal, David E, Donovan, Jenny L, Hamdy, Freddie C, Pharoah, Paul, Pashayan, Nora, Khaw, Kay-Tee, Maier, Christiane, Vogel, Walther, Luedeke, Manuel, Herkommer, Kathleen, Kibel, Adam S, Cybulski, Cezary, Wokolorczyk, Dominika, Kluzniak, Wojciech, Cannon-Albright, Lisa, Brenner, Hermann, Cuk, Katarina, Saum, Kai-Uwe, Park, Jong Y, Sellers, Thomas A, Slavov, Chavdar, Kaneva, Radka, Mitev, Vanio, Batra, Jyotsna, Clements, Judith A, Spurdle, Amanda, Teixeira, Manuel R, Paulo, Paula, Maia, Sofia, Pandha, Hardev, Michael, Agnieszka, Kierzek, Andrzej, Karow, David S, Mills, Ian G, Andreassen, Ole A, and Dale, Anders M

55. Genome-wide association study of prostate cancer-specific survival.

Author

Szulkin R, Karlsson R, Whitington T, Aly M, Gronberg H, Eeles RA, Easton DF, Kote-Jarai Z, Al Olama AA, Benlloch S, Muir K, Giles GG, Southey MC, FitzGerald LM, Henderson BE, Schumacher FR, Haiman CA, Sipeky C, Tammela TL, Nordestgaard BG, Key TJ, Travis RC, Neal DE, Donovan JL, Hamdy FC, Pharoah PD, Pashayan N, Khaw KT, Stanford JL, Thibodeau SN, McDonnell SK, Schaid DJ, Maier C, Vogel W, Luedeke M, Herkommer K, Kibel AS, Cybulski C, Lubiński J, Kluźniak W, Cannon-Albright L, Brenner H, Herrmann V, Holleczek B, Park JY, Sellers TA, Lim HY, Slavov C, Kaneva RP, Mitev VI, Spurdle A, Teixeira MR, Paulo P, Maia S, Pandha H, Michael A, Kierzek A, Batra J, Clements JA, Albanes D, Andriole GL, Berndt SI, Chanock S, Gapstur SM, Giovannucci EL, Hunter DJ, Kraft P, Le Marchand L, Ma J, Mondul AM, Penney KL, Stampfer MJ, Stevens VL, Weinstein SJ, Trichopoulou A, Bueno-de-Mesquita BH, Tjønneland A, Cox DG, Maehle L, Schleutker J, Lindström S, and Wiklund F

Subjects
Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide genetics, Prostatic Neoplasms genetics, Survival Analysis, Prostatic Neoplasms mortality
Abstract

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

Published
2015
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