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1. Supplementary Figure 1 from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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2. Supplementary Table 3 from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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3. Data from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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4. Supplementary Table 2 from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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5. Data from Sequence Variants at 22q13 Are Associated with Prostate Cancer Risk

Author

Sun, Jielin, primary, Zheng, Siqun Lilly, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Li, Ge, primary, Wiley, Kathleen E., primary, Kim, Seong-Tae, primary, Zhu, Yi, primary, Zhang, Zheng, primary, Hsu, Fang-Chi, primary, Turner, Aubrey R., primary, Stattin, Pär, primary, Liu, Wennuan, primary, Kim, Jin Woo, primary, Duggan, David, primary, Carpten, John, primary, Isaacs, William, primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Chang, Bao-Li, primary

Published
2023
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6. Supplementary Table 4 from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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7. Supplementary Table 1 from A Novel Prostate Cancer Susceptibility Locus at 19q13

Author

Hsu, Fang-Chi, primary, Sun, Jielin, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Wiley, Kathleen E., primary, Purcell, Lina D., primary, Gao, Zhengrong, primary, Stattin, Pär, primary, Zhu, Yi, primary, Kim, Seong-Tae, primary, Zhang, Zheng, primary, Liu, Wennuan, primary, Chang, Bao-Li, primary, Walsh, Patrick C., primary, Duggan, David, primary, Carpten, John D., primary, Isaacs, William B., primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Zheng, S. Lilly, primary

Published
2023
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8. Supplementary Methods, Tables and Figures from Sequence Variants at 22q13 Are Associated with Prostate Cancer Risk

Author

Sun, Jielin, primary, Zheng, Siqun Lilly, primary, Wiklund, Fredrik, primary, Isaacs, Sarah D., primary, Li, Ge, primary, Wiley, Kathleen E., primary, Kim, Seong-Tae, primary, Zhu, Yi, primary, Zhang, Zheng, primary, Hsu, Fang-Chi, primary, Turner, Aubrey R., primary, Stattin, Pär, primary, Liu, Wennuan, primary, Kim, Jin Woo, primary, Duggan, David, primary, Carpten, John, primary, Isaacs, William, primary, Grönberg, Henrik, primary, Xu, Jianfeng, primary, and Chang, Bao-Li, primary

Published
2023
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9. Genome-wide association of familial prostate cancer cases identifies evidence for a rare segregating haplotype at 8q24.21

Author

Teerlink, Craig C., Leongamornlert, Daniel, Dadaev, Tokhir, Thomas, Alun, Farnham, James, Stephenson, Robert A., Riska, Shaun, McDonnell, Shannon K., Schaid, Daniel J., Catalona, William J., Zheng, S. Lilly, Cooney, Kathleen A., Ray, Anna M., Zuhlke, Kimberly A., Lange, Ethan M., Giles, Graham G., Southey, Melissa C., Fitzgerald, Liesel M., Rinckleb, Antje, Luedeke, Manuel, Maier, Christiane, Stanford, Janet L., Ostrander, Elaine A., Kaikkonen, Elina M., Sipeky, Csilla, Tammela, Teuvo, Schleutker, Johanna, Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Isaacs, William B., Xu, Jianfeng, Cancel-Tassin, Geraldine, Cussenot, Olivier, Mandal, Diptasri, Laurie, Cecelia, Laurie, Cathy, Thibodeau, Stephen N., Eeles, Rosalind A., Kote-Jarai, Zsofia, Cannon-Albright, Lisa, The PRACTICAL consortium, and International Consortium for Prostate Cancer Genetics

Published
2016
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11. Association analysis of 9,560 prostate cancer cases from the International Consortium of Prostate Cancer Genetics confirms the role of reported prostate cancer associated SNPs for familial disease

Author

Teerlink, Craig C., Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., Rinckleb, Antje, Maier, Christiane, Vogel, Walther, Cancel-Tassin, Geraldine, Egrot, Christophe, Cussenot, Olivier, Foulkes, William D., Giles, Graham G., Hopper, John L., Severi, Gianluca, Eeles, Ros, Easton, Douglas, Kote-Jarai, Zsofia, Guy, Michelle, Cooney, Kathleen A., Ray, Anna M., Zuhlke, Kimberly A., Lange, Ethan M., FitzGerald, Liesel M., Stanford, Janet L., Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Isaacs, William B., Wahlfors, Tiina, Tammela, Teuvo, Schleutker, Johanna, Wiklund, Fredrik, Grönberg, Henrik, Emanuelsson, Monica, Carpten, John, Bailey-Wilson, Joan, Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Catalona, William J., Zheng, S. Lilly, Jin, Guangfu, Lu, Lingyi, Xu, Jianfeng, Camp, Nicola J., Cannon-Albright, Lisa A., and International Consortium for Prostate Cancer Genetics

Published
2014
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12. HOXB13 is a susceptibility gene for prostate cancer: results from the International Consortium for Prostate Cancer Genetics (ICPCG)

Author

Xu, Jianfeng, Lange, Ethan M., Lu, Lingyi, Zheng, Siqun L., Wang, Zhong, Thibodeau, Stephen N., Cannon-Albright, Lisa A., Teerlink, Craig C., Camp, Nicola J., Johnson, Anna M., Zuhlke, Kimberly A., Stanford, Janet L., Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Maier, Christiane, Luedeke, Manuel, Vogel, Walther, Schleutker, Johanna, Wahlfors, Tiina, Tammela, Teuvo, Schaid, Daniel, McDonnell, Shannon K., DeRycke, Melissa S., Cancel-Tassin, Geraldine, Cussenot, Olivier, Wiklund, Fredrik, Grönberg, Henrik, Eeles, Ros, Easton, Doug, Kote-Jarai, Zsofia, Whittemore, Alice S., Hsieh, Chih-Lin, Giles, Graham G., Hopper, John L., Severi, Gianluca, Catalona, William J., Mandal, Diptasri, Ledet, Elisa, Foulkes, William D., Hamel, Nancy, Mahle, Lovise, Moller, Pal, Powell, Isaac, Bailey-Wilson, Joan E., Carpten, John D., Seminara, Daniela, Cooney, Kathleen A., Isaacs, William B., and International Consortium for Prostate Cancer Genetics

Published
2013
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13. Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)

Author

Jin, Guangfu, Lu, Lingyi, Cooney, Kathleen A., Ray, Anna M., Zuhlke, Kimberly A., Lange, Ethan M., Cannon-Albright, Lisa A., Camp, Nicola J., Teerlink, Craig C., FitzGerald, Liesel M., Stanford, Janet L., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Foulkes, William D., Giles, Graham G., Hopper, John L., Severi, Gianluca, Eeles, Ros, Easton, Doug, Kote-Jarai, Zsofia, Guy, Michelle, Rinckleb, Antje, Maier, Christiane, Vogel, Walther, Cancel-Tassin, Geraldine, Egrot, Christophe, Cussenot, Olivier, Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., Wiklund, Fredrik, Grönberg, Henrik, Emanuelsson, Monica, Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Wahlfors, Tiina, Tammela, Teuvo, Schleutker, Johanna, Catalona, William J., Zheng, S. Lilly, Ostrander, Elaine A., Isaacs, William B., Xu, Jianfeng, and International Consortium for Prostate Cancer Genetics

Published
2012
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14. Two-locus genome-wide linkage scan for prostate cancer susceptibility genes with an interaction effect

Author

Chang, Bao-Li, Lange, Ethan M., Dimitrov, Latchezar, Valis, Christopher J., Gillanders, Elizabeth M., Lange, Leslie A., Wiley, Kathleen E., Isaacs, Sarah D., Wiklund, Fredrik, Baffoe-Bonnie, Agnes, Langefeld, Carl D, Zheng, S. Lilly, Matikainen, Mika P., Ikonen, Tarja, Fredriksson, Henna, Tammela, Teuvo, Walsh, Patrick C., Bailey-Wilson, Joan E., Schleutker, Johanna, Gronberg, Henrik, Cooney, Kathleen A., Isaacs, William B., Suh, Edward, Trent, Jeffrey M., and Xu, Jianfeng

Published
2006
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15. A combined genomewide linkage scan of 1,233 families for prostate cancer-susceptibility genes conducted by the International Consortium for Prostate Cancer Genetics

Author

Xu, Jianfeng, Dimitrov, Latchezar, Chang, Bao-Li, Adams, Tamara S., Turner, Aubrey R., Meyers, Deborah A., Eeles, Rosalind A., Easton, Douglas F., Foulkes, William D., Simard, Jacques, Giles, Graham G., Hopper, John L., Mahle, Lovise, Moller, Pal, Bishop, Tim, Evans, Chris, Edwards, Steve, Meitz, Julia, Bullock, Sarah, Hope, Questa, Hsieh, Chih-lin, Halpern, Jerry, Balise, Raymond N., Oakley-Girvan, Ingrid, Whittemore, Alice S., Ewing, Charles M., Gielzak, Marta, Isaacs, Sarah D., Walsh, Patrick C., Wiley, Kathleen E., Isaacs, William B., Thibodeau, Stephen N., McDonnell, Shannon K., Cunningham, Julie M., Zarfas, Katherine E., Hebbring, Scott, Schaid, Daniel J., Friedrichsen, Danielle M., Deutsch, Kerry, Kolb, Suzanne, Badzioch, Michael, Jarvik, Gail P., Janer, Marta, Hood, Leroy, Ostrander, Elaine A., Stanford, Janet L., Lange, Ethan M., Beebe-Dimmer, Jennifer L., Mohai, Caroline E., Cooney, Kathleen A., Ikonen, Tarja, Baffoe-Bonnie, Agnes, Fredriksson, Henna, Matikainen, Mika P., Tammela, Teuvo LJ, Bailey-Wilson, Joan, Schleutker, Johanna, Maier, Christiane, Herkommer, Kathleen, Hoegel, Josef J., Vogel, Walther, Paiss, Thomas, Wiklund, Fredrik, Emanuelsson, Monica, Stenman, Elisabeth, Jonsson, Bjorn-Anders, Gronberg, Henrik, Camp, Nicola J., Farnham, James, Cannon-Albright, Lisa A., and Seminara, Daniela

Subjects
Prostate cancer -- Genetic aspects, Human genetics -- Research, Biological sciences
Published
2005

16. Common sequence variants of the macrophage scavenger receptor 1 gene are associated with prostate cancer risk

Author

Xu, Jianfeng, Zheng, S. Lilly, Komiya, Akira, Mychaleckyj, Josyf C., Isaacs, Sara D., Chang, Baoli, Turner, Aubrey R., Ewing, Charles M., Wiley, Kathleen E., Hawkins, Gregory A., Bleecker, Eugene R., Walsh, Patrick C., Meyers, Deborah A., and Isaacs, William B.

Subjects
Macrophages -- Physiological aspects, Macrophages -- Genetic aspects, Prostate cancer -- Physiological aspects, Prostate cancer -- Genetic aspects, Gene mutations -- Physiological aspects, Gene mutations -- Health aspects, Biological sciences
Published
2003

17. Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG

Author

Lu, Lingyi, Cancel-Tassin, Geraldine, Valeri, Antoine, Cussenot, Olivier, Lange, Ethan M., Cooney, Kathleen A., Farnham, James M., Camp, Nicola J., Cannon-Albright, Lisa A., Tammela, Teuvo L.J., Schleutker, Johanna, Hoegel, Josef, Herkommer, Kathleen, Maier, Christiane, Vogel, Walther, Wiklund, Fredrik, Emanuelsson, Monica, Grönberg, Henrik, Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Helfand, Brian T., Kan, Donghui, Catalona, William J., Stanford, Janet L., FitzGerald, Liesel M., Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A., Thibodeau, Stephen N., McDonnell, Shannon K., Hebbring, Scott, Schaid, Daniel J., Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Powell, Isaac, Bailey-Wilson, Joan E., Cropp, Cheryl D., Simpson, Claire, Carpten, John D., Seminara, Daniela, Zheng, Lilly S., Xu, Jianfen, Giles, Graham G., Severi, Gianluca, Hopper, John L., English, Dallas R., Foulkes, William D., Maehle, Lovise, Moller, Pal, Badzioch, Michael D., Edwards, Steve, Guy, Michelle, Eeles, Ros, Easton, Douglas, and Isaacs, William B.

Published
2012
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18. Germline Mutations in HOXB13 and Prostate-Cancer Risk

Author

Ewing, Charles M., Ray, Anna M., Lange, Ethan M., Zuhlke, Kimberly A., Robbins, Christiane M., Tembe, Waibhav D., Wiley, Kathleen E., Isaacs, Sarah D., Johng, Dorhyun, Wang, Yunfei, Bizon, Chris, Yan, Guifang, Gielzak, Marta, Partin, Alan W., Shanmugam, Vijayalakshmi, Izatt, Tyler, Sinari, Shripad, Craig, David W., Zheng, Lilly S., Walsh, Patrick C., Montie, James E., Xu, Jianfeng, Carpten, John D., Isaacs, William B., and Cooney, Kathleen A.

Published
2012
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20. Large-scale fine mapping of the HNF1B locus and prostate cancer risk

Author

Berndt, Sonja I., Sampson, Joshua, Yeager, Meredith, Jacobs, Kevin B., Wang, Zhaoming, Hutchinson, Amy, Chung, Charles, Orr, Nick, Wacholder, Sholom, Chatterjee, Nilanjan, Yu, Kai, Kraft, Peter, Feigelson, Heather Spencer, Thun, Michael J., Diver, W. Ryan, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Schumacher, Fredrick R., Cancel-Tassin, Geraldine, Cussenot, Olivier, Valeri, Antoine, Andriole, Gerald L., Crawford, E. David, Haiman, Christopher, Henderson, Brian, Kolonel, Laurence, Le Marchand, Loic, Siddiq, Afshan, Riboli, Elio, Travis, Ruth C., Kaaks, Rudolf, Isaacs, William, Isaacs, Sarah, Wiley, Kathleen E., Gronberg, Henrik, Wiklund, Fredrik, Stattin, Pär, Xu, Jianfeng, Zheng, S. Lilly, Sun, Jielin, Vatten, Lars J., Hveem, Kristian, Njølstad, Inger, Gerhard, Daniela S., Tucker, Margaret, Hayes, Richard B., Hoover, Robert N., Fraumeni, Joseph F., Jr, Hunter, David J., Thomas, Gilles, and Chanock, Stephen J.

Published
2011
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21. Genome-Wide Linkage Analysis of 1,233 Prostate Cancer Pedigrees From the International Consortium for Prostate Cancer Genetics Using Novel sum LINK and sum LOD Analyses

Author

Christensen, Bryce G., Baffoe-Bonnie, Agnes B., George, Asha, Powell, Isaac, Bailey-Wilson, Joan E., Carpten, John D., Giles, Graham G., Hopper, John L., Severi, Gianluca, English, Dallas R., Foulkes, William D., Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D., Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L., Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Isaacs, William B., Thibodeau, Stephen N., McDonnell, Shannon K., Hebbring, Scott, Schaid, Daniel J., Lange, Ethan M., Cooney, Kathleen A., Tammela, Teuvo L.J., Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Grönberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Farnham, James M., Cannon-Albright, Lisa A., and Camp, Nicola J.

Published
2010
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23. Fine mapping association study and functional analysis implicate a SNP in MSMB at 10q11 as a causal variant for prostate cancer risk

Author

Chang, Bao-Li, Cramer, Scott D., Wiklund, Fredrik, Isaacs, Sarah D., Stevens, Victoria L., Sun, Jielin, Smith, Shelly, Pruett, Kristen, Romero, Lina M., Wiley, Kathleen E., Kim, Seong-Tae, Zhu, Yi, Zhang, Zheng, Hsu, Fang-Chi, Turner, Aubrey R., Adolfsson, Jan, Liu, Wennuan, Kim, Jin Woo, Duggan, David, Carpten, John, Zheng, S Lilly, Rodriguez, Carmen, Isaacs, William B., Grönberg, Henrik, and Xu, Jianfeng

Published
2009

27. Two Genome-wide Association Studies of Aggressive Prostate Cancer Implicate Putative Prostate Tumor Suppressor Gene DAB2IP

Author

Duggan, David, Zheng, Siqun L., Knowlton, Michele, Benitez, Debbie, Dimitrov, Latchezar, Wiklund, Fredrik, Robbins, Christiane, Isaacs, Sarah D., Cheng, Yu, Li, Ge, Sun, Jielin, Chang, Bao-Li, Marovich, Leslie, Wiley, Kathleen E., Bälter, Katarina, Stattin, Pär, Adami, Hans-Olov, Gielzak, Marta, Yan, Guifang, Sauvageot, Jurga, Liu, Wennuan, Kim, Jin Woo, Bleecker, Eugene R., Meyers, Deborah A., Trock, Bruce J., Partin, Alan W., Walsh, Patrick C., Isaacs, William B., Grönberg, Henrik, Xu, Jianfeng, and Carpten, John D.

Published
2007

29. Association Between Two Unlinked Loci at 8q24 and Prostate Cancer Risk Among European Americans

Author

Zheng, S. Lilly, Sun, Jielin, Cheng, Yu, Li, Ge, Hsu, Fang-Chi, Zhu, Yi, Chang, Bao-Li, Liu, Wennuan, Kim, Jin Woo, Turner, Aubrey R., Gielzak, Marta, Yan, Guifang, Isaacs, Sarah D., Wiley, Kathleen E., Sauvageot, Jurga, Chen, Huann-Sheng, Gurganus, Robin, Mangold, Leslie A., Trock, Bruce J., Gronberg, Henrik, Duggan, David, Carpten, John D., Partin, Alan W., Walsh, Patrick C., Xu, Jianfeng, and Isaacs, William B.

Published
2007

30. Compelling evidence for a prostate cancer gene at 22q12.3 by the International Consortium for Prostate Cancer Genetics

Author

Camp, Nicola J., Cannon-Albright, Lisa A., Farnham, James M., Baffoe-Bonnie, Agnes B., George, Asha, Powell, Isaac, Bailey-Wilson, Joan E., Carpten, John D., Giles, Graham G., Hopper, John L., Severi, Gianluca, English, Dallas R., Foulkes, William D., Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D., Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L., Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Thibodeau, Stephen N., McDonnell, Shannon K., Hebbring, Scott, Schaid, Daniel J., Lange, Ethan M., Cooney, Kathleen A., Tammela, Teuvo L.J., Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Grönberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, and Isaacs, William B.

Published
2007

32. Combined Genome-Wide Scan for Prostate Cancer Susceptibility Genes

Author

Gillanders, Elizabeth M., Xu, Jianfeng, Chang, Bao-li, Lange, Ethan M., Wiklund, Fredrik, Bailey-Wilson, Joan E., Baffoe-Bonnie, Agnes, Jones, MaryPat, Gildea, Derek, Riedesel, Erica, Albertus, Julie, Isaacs, Sarah D., Wiley, Kathleen E., Mohai, Caroline E., Matikainen, Mika P., Tammela, Teuvo L. J., Zheng, S. Lilly, Brown, W. Mark, Rökman, Annika, Carpten, John D., Meyers, Deborah A., Walsh, Patrick C., Schleutker, Johanna, Gronberg, Henrik, Cooney, Kathleen A., Isaacs, William B., and Trent, Jeffrey M.

Published
2004

33. Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families

Author

Bailey-Wilson Joan E, Childs Erica J, Cropp Cheryl D, Schaid Daniel J, Xu Jianfeng, Camp Nicola J, Cannon-Albright Lisa A, Farnham James M, George Asha, Powell Isaac, Carpten John D, Giles Graham G, Hopper John L, Severi Gianluca, English Dallas R, Foulkes William D, Mæhle Lovise, Møller Pål, Eeles Rosalind, Easton Douglas, Guy Michelle, Edwards Steve, Badzioch Michael D, Whittemore Alice S, Oakley-Girvan Ingrid, Hsieh Chih-Lin, Dimitrov Latchezar, Stanford Janet L, Karyadi Danielle M, Deutsch Kerry, McIntosh Laura, Ostrander Elaine A, Wiley Kathleen E, Isaacs Sarah D, Walsh Patrick C, Thibodeau Stephen N, McDonnell Shannon K, Hebbring Scott, Lange Ethan M, Cooney Kathleen A, Tammela Teuvo LJ, Schleutker Johanna, Maier Christiane, Bochum Sylvia, Hoegel Josef, Grönberg Henrik, Wiklund Fredrik, Emanuelsson Monica, Cancel-Tassin Geraldine, Valeri Antoine, Cussenot Olivier, and Isaacs William B

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive. Methods Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed. Results Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2–3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded. Conclusions Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2–3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region.

Published
2012
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35. Common colorectal cancer risk alleles contribute to the multiple colorectal adenoma phenotype, but do not influence colonic polyposis in FAP

Author

Cheng, Timothy H. T, Gorman, Maggie, Martin, Lynn, Barclay, Ella, Casey, Graham, Newcomb, Polly A., Conti, David V., Schumacher, Fred, Gallinger, Steve, Lindor, Noralane M., Hopper, John, Jenkins, Mark, Hunter, David J., Kraft, Peter, Jacobs, Kevin B., Cox, David G., Yeager, Meredith, Hankinson, Susan E., Wacholder, Sholom, Wang, Zhaoming, Welch, Robert, Hutchinson, Amy, Wang, Junwen, Yu, Kai, Chatterjee, Nilanjan, Orr, Nick, Willett, Walter C., Colditz, Graham A., Ziegler, Regina G., Berg, Christine D., Buys, Saundra S., Mccarty, Catherine A., Feigelson, Heather Spencer, Calle, Eugenia E., Thun, Michael J., Hayes, Richard B., Tucker, Margaret, Gerhard, Daniela S., Fraumeni, Joseph F., Hoover, Robert N., Thomas, Gilles, Chanock, Stephen J., Ciampa, Julia, Gonzalez Bosquet, Jesus, Berndt, Sonja, Amundadottir, Laufey, Diver, W. Ryan, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Schumacher, Fredrick R., Cancel Tassin, Geraldine, Cussenot, Olivier, Valeri, Antoine, Andriole, Gerald L., Crawford, E. David, Haiman, Christopher A., Henderson, Brian, Kolonel, Laurence, Marchand, Loic Le, Siddiq, Afshan, Riboli, Elio, Key, Timothy J., Kaaks, Rudolf, Isaacs, William, Isaacs, Sarah, Wiley, Kathleen E., Gronberg, Henrik, Wiklund, Fredrik, Stattin, Pär, Xu, Jianfeng, Zheng, S. Lilly, Sun, Jielin, Vatten, Lars J., Hveem, Kristian, Kumle, Merethe, Purdue, Mark P., Johansson, Mattias, Zelenika, Diana, Toro, Jorge R., Scelo, Ghislaine, Moore, Lee E., Prokhortchouk, Egor, Wu, Xifeng, Kiemeney, Lambertus A., Gaborieau, Valerie, Chow, Wong Ho, Zaridze, David, Matveev, Vsevolod, Lubinski, Jan, Trubicka, Joanna, Szeszenia Dabrowska, Neonila, Lissowska, Jolanta, Rudnai, Péter, Fabianova, Eleonora, Bucur, Alexandru, Bencko, Vladimir, Foretova, Lenka, Janout, Vladimir, Boffetta, Paolo, Colt, Joanne S., Davis, Faith G., Schwartz, Kendra L., Banks, Rosamonde E., Selby, Peter J., Harnden, Patricia, Hsing, Ann W., Grubb, Robert L., Boeing, Heiner, Vineis, Paolo, Clavel Chapelon, Franc¸oise, Palli, Domenico, Tumino, Rosario, Krogh, Vittorio, Duell, Eric J., Quirós, José Ramón, Sanchez, Maria José, Navarro, Carmen, Ardanaz, Eva, Dorronsoro, Miren, Khaw, Kay Tee, Allen, Naomi E., Bueno de Mesquita, H. Bas, Peeters, Petra H. M., Trichopoulos, Dimitrios, Linseisen, Jakob, Ljungberg, Börje, Overvad, Kim, Tjønneland, Anne, Romieu, Isabelle, Mukeria, Anush, Shangina, Oxana, Stevens, Victoria L., Gapstur, Susan M., Pharoah, Paul D., Easton, Douglas F., Weinstein, Stephanie J., Njølstad, Inger, Tell, Grethe S., Stoltenberg, Camilla, Kumar, Rajiv, Koppova, Kvetoslava, Benhamou, Simone, Oosterwijk, Egbert, Vermeulen, Sita H., Aben, Katja K. H., Van Der Marel, Saskia L., Ye, Yuanqing, Wood, Christopher G., Pu, Xia, Mazur, Alexander M., Boulygina, Eugenia S., Chekanov, Nikolai N., Foglio, Mario, Lechner, Doris, Gut, Ivo, Heath, Simon, Blanche, Hélène, Skryabin, Konstantin G., Mckay, James D., Rothman, Nathaniel, Lathrop, Mark, Brennan, Paul, Saunders, Brian, Thomas, Huw, Clark, Sue, Tomlinson, Ian, PANICO, SALVATORE, Cheng, Timothy H. T, Gorman, Maggie, Martin, Lynn, Barclay, Ella, Casey, Graham, Newcomb, Polly A., Conti, David V., Schumacher, Fred, Gallinger, Steve, Lindor, Noralane M., Hopper, John, Jenkins, Mark, Hunter, David J., Kraft, Peter, Jacobs, Kevin B., Cox, David G., Yeager, Meredith, Hankinson, Susan E., Wacholder, Sholom, Wang, Zhaoming, Welch, Robert, Hutchinson, Amy, Wang, Junwen, Yu, Kai, Chatterjee, Nilanjan, Orr, Nick, Willett, Walter C., Colditz, Graham A., Ziegler, Regina G., Berg, Christine D., Buys, Saundra S., Mccarty, Catherine A., Feigelson, Heather Spencer, Calle, Eugenia E., Thun, Michael J., Hayes, Richard B., Tucker, Margaret, Gerhard, Daniela S., Fraumeni, Joseph F., Hoover, Robert N., Thomas, Gille, Chanock, Stephen J., Ciampa, Julia, Gonzalez Bosquet, Jesu, Berndt, Sonja, Amundadottir, Laufey, Diver, W. Ryan, Albanes, Demetriu, Virtamo, Jarmo, Weinstein, Stephanie, Schumacher, Fredrick R., Cancel Tassin, Geraldine, Cussenot, Olivier, Valeri, Antoine, Andriole, Gerald L., Crawford, E. David, Haiman, Christopher A., Henderson, Brian, Kolonel, Laurence, Marchand, Loic Le, Siddiq, Afshan, Riboli, Elio, Key, Timothy J., Kaaks, Rudolf, Isaacs, William, Isaacs, Sarah, Wiley, Kathleen E., Gronberg, Henrik, Wiklund, Fredrik, Stattin, Pär, Xu, Jianfeng, Zheng, S. Lilly, Sun, Jielin, Vatten, Lars J., Hveem, Kristian, Kumle, Merethe, Purdue, Mark P., Johansson, Mattia, Zelenika, Diana, Toro, Jorge R., Scelo, Ghislaine, Moore, Lee E., Prokhortchouk, Egor, Wu, Xifeng, Kiemeney, Lambertus A., Gaborieau, Valerie, Chow, Wong Ho, Zaridze, David, Matveev, Vsevolod, Lubinski, Jan, Trubicka, Joanna, Szeszenia Dabrowska, Neonila, Lissowska, Jolanta, Rudnai, Péter, Fabianova, Eleonora, Bucur, Alexandru, Bencko, Vladimir, Foretova, Lenka, Janout, Vladimir, Boffetta, Paolo, Colt, Joanne S., Davis, Faith G., Schwartz, Kendra L., Banks, Rosamonde E., Selby, Peter J., Harnden, Patricia, Hsing, Ann W., Grubb, Robert L., Boeing, Heiner, Vineis, Paolo, Clavel Chapelon, Franc¸oise, Palli, Domenico, Tumino, Rosario, Krogh, Vittorio, Panico, Salvatore, Duell, Eric J., Quirós, José Ramón, Sanchez, Maria José, Navarro, Carmen, Ardanaz, Eva, Dorronsoro, Miren, Khaw, Kay Tee, Allen, Naomi E., Bueno de Mesquita, H. Ba, Peeters, Petra H. M., Trichopoulos, Dimitrio, Linseisen, Jakob, Ljungberg, Börje, Overvad, Kim, Tjønneland, Anne, Romieu, Isabelle, Mukeria, Anush, Shangina, Oxana, Stevens, Victoria L., Gapstur, Susan M., Pharoah, Paul D., Easton, Douglas F., Weinstein, Stephanie J., Njølstad, Inger, Tell, Grethe S., Stoltenberg, Camilla, Kumar, Rajiv, Koppova, Kvetoslava, Benhamou, Simone, Oosterwijk, Egbert, Vermeulen, Sita H., Aben, Katja K. H., Van Der Marel, Saskia L., Ye, Yuanqing, Wood, Christopher G., Pu, Xia, Mazur, Alexander M., Boulygina, Eugenia S., Chekanov, Nikolai N., Foglio, Mario, Lechner, Dori, Gut, Ivo, Heath, Simon, Blanche, Hélène, Skryabin, Konstantin G., Mckay, James D., Rothman, Nathaniel, Lathrop, Mark, Brennan, Paul, Saunders, Brian, Thomas, Huw, Clark, Sue, and Tomlinson, Ian

Subjects
Adenoma, Allele, Male, Genes, Modifier, Adenomatous Polyposis Coli Protein, Colorectal Neoplasm, Middle Aged, Polymorphism, Single Nucleotide, Phenotype, Adenomatous Polyposis Coli, Genetics, Female, Genetic Predisposition to Disease, DNA Glycosylase, Germ-Line Mutation, Genetics (clinical), Aged, Human
Abstract

The presence of multiple (5-100) colorectal adenomas suggests an inherited predisposition, but the genetic aetiology of this phenotype is undetermined if patients test negative for Mendelian polyposis syndromes such as familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). We investigated whether 18 common colorectal cancer (CRC) predisposition single-nucleotide polymorphisms (SNPs) could help to explain some cases with multiple adenomas who phenocopied FAP or MAP, but had no pathogenic APC or MUTYH variant. No multiple adenoma case had an outlying number of CRC SNP risk alleles, but multiple adenoma patients did have a significantly higher number of risk alleles than population controls (P=5.7 × 10(-7)). The association was stronger in those with ≥10 adenomas. The CRC SNPs accounted for 4.3% of the variation in multiple adenoma risk, with three SNPs (rs6983267, rs10795668, rs3802842) explaining 3.0% of the variation. In FAP patients, the CRC risk score did not differ significantly from the controls, as we expected given the overwhelming effect of pathogenic germline APC variants on the phenotype of these cases. More unexpectedly, we found no evidence that the CRC SNPs act as modifier genes for the number of colorectal adenomas in FAP patients. In conclusion, common colorectal tumour risk alleles contribute to the development of multiple adenomas in patients without pathogenic germline APC or MUTYH variants. This phenotype may have 'polygenic' or monogenic origins. The risk of CRC in relatives of multiple adenoma cases is probably much lower for cases with polygenic disease, and this should be taken into account when counselling such patients.

Published
2015

36. Germline mutations in PPFIBP2 are associated with lethal prostate cancer

Author

Wu, Yishuo, primary, Yu, Hongjie, additional, Zheng, Siqun Lilly, additional, Feng, Bingjian, additional, Kapron, Ashley L., additional, Na, Rong, additional, Boyle, Julie L., additional, Shah, Sameep, additional, Shi, Zhuqing, additional, Ewing, Charles M., additional, Wiley, Kathleen E., additional, Luo, Jun, additional, Walsh, Patrick C., additional, Carter, Herbert Ballentine, additional, Helfand, Brian T., additional, Cooney, Kathleen A., additional, Xu, Jianfeng, additional, and Isaacs, William B., additional

Published
2018
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37. Germline Mutations in ATM and BRCA1/2 Distinguish Risk for Lethal and Indolent Prostate Cancer and are Associated with Early Age at Death

Author

Na, Rong, primary, Zheng, S. Lilly, additional, Han, Misop, additional, Yu, Hongjie, additional, Jiang, Deke, additional, Shah, Sameep, additional, Ewing, Charles M., additional, Zhang, Liti, additional, Novakovic, Kristian, additional, Petkewicz, Jacqueline, additional, Gulukota, Kamalakar, additional, Helseth Jr, Donald L., additional, Quinn, Margo, additional, Humphries, Elizabeth, additional, Wiley, Kathleen E., additional, Isaacs, Sarah D., additional, Wu, Yishuo, additional, Liu, Xu, additional, Zhang, Ning, additional, Wang, Chi-Hsiung, additional, Khandekar, Janardan, additional, Hulick, Peter J., additional, Shevrin, Daniel H., additional, Cooney, Kathleen A., additional, Shen, Zhoujun, additional, Partin, Alan W., additional, Carter, H. Ballentine, additional, Carducci, Michael A., additional, Eisenberger, Mario A., additional, Denmeade, Sam R., additional, McGuire, Michael, additional, Walsh, Patrick C., additional, Helfand, Brian T., additional, Brendler, Charles B., additional, Ding, Qiang, additional, Xu, Jianfeng, additional, and Isaacs, William B., additional

Published
2017
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38. Linkage and Association Studies of Prostate Cancer Susceptibility: Evidence for Linkage at 8p22-23

Author

Xu, Jianfeng, Zheng, Siqun L., Hawkins, Gregory A., Faith, Dennis A., Kelly, Brian, Isaacs, Sarah D., Wiley, Kathleen E., Chang, Bao-li, Ewing, Charles M., Bujnovszky, Piroska, Carpten, John D., Bleecker, Eugene R., Walsh, Patrick C., Trent, Jeffrey M., Meyers, Deborah A., and Isaacs, William B.

Subjects
Prostate cancer -- Genetic aspects, Linkage (Genetics) -- Analysis, Gene expression -- Research, Biological sciences
Published
2001

39. Evaluation of Linkage and Association of HPC2/ELAC2 in Patients with Familial or Sporadic Prostate Cancer

Author

Xu, Jianfeng, Zheng, Siqun L., Carpten, John D., Nupponen, Nina N., Robbins, Christiane M., Mestre, Juanita, Moses, Tracy Y., Faith, Dennis A., Kelly, Brian D., Isaacs, Sarah D., Wiley, Kathleen E., Ewing, Charles M., Bujnovszky, Piroska, Chang, Bao-li, Bailey-Wilson, Joan, Bleecker, Eugene R., Walsh, Patrick C., Trent, Jeffrey M., Meyers, Deborah A., and Isaacs, William B.

Subjects
Prostate cancer -- Genetic aspects, Genetic research -- Analysis, Genetic polymorphisms -- Research, Biological sciences
Published
2001

40. Association analysis of 9,560 prostate cancer cases from the International Consortium of Prostate Cancer Genetics confirms the role of reported prostate cancer associated SNPs for familial disease

Author

Tammela, Teuvo, Ray, Anna M., Cooney, Kathleen A., Easton, Douglas, Maier, Christiane, Cancel-Tassin, Geraldine, Severi, Gianluca, Egrot, Christophe, McDonnell, Shannon K., Rinckleb, Antje, Foulkes, William D., Isaacs, William B., Lange, Ethan M., Schleutker, Johanna, Stanford, Janet L., Schaid, Daniel J., Isaacs, Sarah D., Thibodeau, Stephen N., Vogel, Walther, Giles, Graham G., Kote-Jarai, Zsofia, Eeles, Ros, Cussenot, Olivier, Guy, Michelle, Teerlink, Craig C., Wahlfors, Tiina, Ostrander, Elaine A., Zuhlke, Kimberly A., Hopper, John L., FitzGerald, Liesel M., Wiley, Kathleen E., and Walsh, Patrick C.

Abstract

Previous GWAS studies have reported significant associations between various common SNPs and prostate cancer risk using cases unselected for family history. How these variants influence risk in familial prostate cancer is not well studied. Here, we analyzed 25 previously reported SNPs across 14 loci from prior prostate cancer GWAS. The International Consortium for Prostate Cancer Genetics (ICPCG) previously validated some of these using a family-based association method (FBAT). However, this approach suffered reduced power due to the conditional statistics implemented in FBAT. Here, we use a case-control design with an empirical analysis strategy to analyze the ICPCG resource for association between these 25 SNPs and familial prostate cancer risk. Fourteen sites contributed 12,506 samples (9,560 prostate cancer cases, 3,368 with aggressive disease, and 2,946 controls from 2,283 pedigrees). We performed association analysis with Genie software which accounts for relationships. We analyzed all familial prostate cancer cases and the subset of aggressive cases. For the familial prostate cancer phenotype, 20 of the 25 SNPs were at least nominally associated with prostate cancer and 16 remained significant after multiple testing correction (p≤1E−3) occurring on chromosomal bands 6q25, 7p15, 8q24, 10q11, 11q13, 17q12, 17q24, and Xp11. For aggressive disease, 16 of the SNPs had at least nominal evidence and 8 were statistically significant including 2p15. The results indicate that the majority of common, low-risk alleles identified in GWAS studies for all prostate cancer also contribute risk for familial prostate cancer, and that some may be contribute risk to aggressive disease.

Published
2014
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41. Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families

Author

Bailey-Wilson, Joan E, Childs, Erica J, Cropp, Cheryl D, Schaid, Daniel J, Xu, Jianfeng, Camp, Nicola J, Cannon-Albright, Lisa A, Farnham, James M, George, Asha, Powell, Isaac, Carpten, John D, Giles, Graham G, Hopper, John L, Severi, Gianluca, English, Dallas R, Foulkes, William D, Mæhle, Lovise, Møller, Pål, Eeles, Rosalind, Easton, Douglas, Guy, Michelle, Edwards, Steve, Badzioch, Michael D, Whittemore, Alice S, Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Stanford, Janet L, Karyadi, Danielle M, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A, Wiley, Kathleen E, Isaacs, Sarah D, Walsh, Patrick C, Thibodeau, Stephen N, McDonnell, Shannon K, Hebbring, Scott, Lange, Ethan M, Cooney, Kathleen A, Tammela, Teuvo LJ, Schleutker, Johanna, Maier, Christiane, Bochum, Sylvia, Hoegel, Josef, Grönberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Cancel-Tassin, Geraldine, Valeri, Antoine, Cussenot, Olivier, Isaacs, William B, International Consortium for Prostate Cancer Genetics, Easton, Douglas [0000-0003-2444-3247], and Apollo - University of Cambridge Repository

Subjects
Male, Chromosomes, Human, X, Genetic Linkage, Humans, Prostatic Neoplasms, Alleles, Genome-Wide Association Study, Microsatellite Repeats
Abstract

BACKGROUND: Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive. METHODS: Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed. RESULTS: Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2-3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded. CONCLUSIONS: Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2-3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region.

Published
2012

42. Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG

Author

Kan, Donghui, Tammela, Teuvo L.J., Maier, Christiane, Vogel, Walther, Cancel-Tassin, Geraldine, Isaacs, Sarah D., Valeri, Antoine, Farnham, James M., Thibodeau, Stephen N., Hoegel, Josef, Wiley, Kathleen E., Ostrander, Elaine A., Helfand, Brian T., McIntosh, Laura, Deutsch, Kerry, Lange, Ethan M., Camp, Nicola J., Johanneson, Bo, Cussenot, Olivier, Herkommer, Kathleen, Catalona, William J., Cannon-Albright, Lisa A., Emanuelsson, Monica, Walsh, Patrick C., McDonnell, Shannon K., FitzGerald, Liesel M., Wiklund, Fredrik, Stanford, Janet L., Lu, Lingyi, Schleutker, Johanna, Cooney, Kathleen A., and Grönberg, Henrik

Abstract

In spite of intensive efforts, understanding of the genetic aspects of familial prostate cancer remains largely incomplete. In a previous microsatellite-based linkage scan of 1233 prostate cancer (PC) families, we identified suggestive evidence for linkage (i.e. LOD≥1.86) at 5q12, 15q11, 17q21, 22q12, and two loci on 8p, with additional regions implicated in subsets of families defined by age at diagnosis, disease aggressiveness, or number of affected members.

Published
2012
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43. Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)

Author

Schaid, Daniel J., Cancel-Tassin, Geraldine, Jin, Guangfu, Teerlink, Craig C., FitzGerald, Liesel M., Severi, Gianluca, Lange, Ethan M., Walsh, Patrick C., Camp, Nicola J., Cannon-Albright, Lisa A., Cooney, Kathleen A., Hopper, John L., Egrot, Christophe, Lu, Lingyi, Easton, Doug, Maier, Christiane, Wiley, Kathleen E., Giles, Graham G., Vogel, Walther, Foulkes, William D., Kote-Jarai, Zsofia, Rinckleb, Antje, Stanford, Janet L., Guy, Michelle, Ray, Anna M., Zuhlke, Kimberly A., Eeles, Ros, Thibodeau, Stephen N., Isaacs, Sarah D., Cussenot, Olivier, Wiklund, Fredrik, and McDonnell, Shannon K.

Abstract

Multiple prostate cancer (PCa) risk-related loci have been discovered by genome-wide association studies (GWAS) based on case–control designs. However, GWAS findings may be confounded by population stratification if cases and controls are inadvertently drawn from different genetic backgrounds. In addition, since these loci were identified in cases with predominantly sporadic disease, little is known about their relationships with hereditary prostate cancer (HPC). The association between seventeen reported PCa susceptibility loci was evaluated with a family-based association test using 1,979 hereditary PCa families of European descent collected by members of the International Consortium for Prostate Cancer Genetics, with a total of 5,730 affected men. The risk alleles for 8 of the 17 loci were significantly over-transmitted from parents to affected offspring, including SNPs residing in 8q24 (regions 1, 2 and 3), 10q11, 11q13, 17q12 (region 1), 17q24 and Xp11. In subgroup analyses, three loci, at 8q24 (regions 1 and 2) plus 17q12, were significantly over-transmitted in hereditary PCa families with five or more affected members, while loci at 3p12, 8q24 (region 2), 11q13, 17q12 (region 1), 17q24 and Xp11 were significantly over-transmitted in HPC families with an average age of diagnosis at 65 years or less. Our results indicate that at least a subset of PCa risk-related loci identified by case–control GWAS are also associated with disease risk in HPC families.

Published
2012
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44. Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for prostate cancer Genetics using novel sumLINK and sumLOD analyses

Author

Hsieh, Chih-Lin, Oakley-Girvan, Ingrid, Easton, Douglas, Severi, Gianluca, Thibodeau, Stephen N., Whittemore, Alice S., Eeles, Ros, Powell, Isaac, Moller, Pal, Giles, Graham G., Foulkes, William D., McIntosh, Laura, Bailey-Wilson, Joan E., Hopper, John L., Deutsch, Kerry, Isaacs, Sarah D., Dimitrov, Latchezar, Isaacs, William B., Johanneson, Bo, Walsh, Patrick C., English, Dallas R., Wiley, Kathleen E., Christensen, G. Bryce, Xu, Jianfeng, Maehle, Lovise, McDonnell, Shannon K., Stanford, Janet L., Baffoe-Bonnie, Agnes B., George, Asha, Badzioch, Michael D., Carpten, John D., and Ostrander, Elaine A.

Abstract

Prostate cancer is generally believed to have a strong inherited component, but the search for susceptibility genes has been hindered by the effects of genetic heterogeneity. The recently developed sumLINK and sumLOD statistics are powerful tools for linkage analysis in the presence of heterogeneity.

Published
2010
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45. Individual and cumulative effect of prostate cancer risk-associated variants on clinicopathologic variables in 5,895 prostate cancer patients

Author

Kader, A. Karim, Sun, Jielin, Isaacs, Sarah D., Wiley, Kathleen E., Yan, Guifang, Kim, Seong-Tae, Fedor, Helen, DeMarzo, Angelo M., Epstein, Jonathan I., Walsh, Patrick C., Partin, Alan W., Trock, Bruce, Zheng, S. Lilly, Xu, Jianfeng, and Isaacs, William

Subjects
Male, Prostatectomy, Genotype, Prostatic Neoplasms, Prostatic Secretory Proteins, Middle Aged, Prostate-Specific Antigen, Polymorphism, Single Nucleotide, Article, Cohort Studies, Gene Frequency, Predictive Value of Tests, Risk Factors, Biomarkers, Tumor, Humans, Genetic Predisposition to Disease, Retrospective Studies
Abstract

More than a dozen single nucleotide polymorphisms (SNPs) have been associated with prostate cancer (PCa) risk from genome-wide association studies (GWAS). Their association with PCa aggressiveness and clinicopathologic variables is inconclusive.Twenty PCa risk SNPs implicated in GWAS and fine mapping studies were evaluated in 5,895 PCa cases treated by radical prostatectomy at Johns Hopkins Hospital, where each tumor was uniformly graded and staged using the same protocol.For 18 of the 20 SNPs examined, no statistically significant differences (P0.05) were observed in risk allele frequencies between patients with more aggressive (Gleason scoresor =4 + 3, or stageor =T3b, or N+) or less aggressive disease (Gleason scoresor =3 + 4, and stageor =T2, and N0). For the two SNPs that had significant differences between more and less aggressive disease rs2735839 in KLK3 (P = 8.4 x 10(-7)) and rs10993994 in MSMB (P = 0.046), the alleles that are associated with increased risk for PCa were more frequent in patients with less aggressive disease. Since these SNPs are known to be associated with PSA levels in men without PCa diagnoses, these latter associations may reflect the enrichment of low grade, low stage cases diagnosed by contemporary disease screening with PSA.The vast majority of PCa risk-associated SNPs are not associated with aggressiveness and clinicopathologic variables of PCa. Correspondingly, they have minimal utility in predicting the risk for developing more or less aggressive forms of PCa.

Published
2009

46. Association of variants at two 17q loci with prostate cancer risk in European and African Americans

Author

Sun, Jielin, Purcell, Lina, Gao, Zhengrong, Isaacs, Sarah D., Wiley, Kathleen E., Hsu, Fang-Chi, Liu, Wennuan, Duggan, David, Carpten, John D., Grönberg, Henrik, Xu, Jianfeng, Chang, Bao-Li, Partin, Alan W., Walsh, Patrick C., Isaacs, William B., and Zheng, S. Lilly

Subjects
Male, Maryland, Prostatic Neoplasms, Middle Aged, Prostate-Specific Antigen, Polymorphism, Single Nucleotide, Risk Assessment, Article, White People, Black or African American, Case-Control Studies, Odds Ratio, Humans, Genetic Predisposition to Disease, Chromosomes, Human, Pair 17
Abstract

Multiple SNPs at 17q12 and 17q24.3 were recently identified to be associated with prostate cancer risk using a genome-wide association study. Although these associations reached genome-wide significance level in a combined analysis of several study populations of European descent in the original report, confirmation in independent populations, including African Americans (AA), is critical to increase confidence that they represent true disease associations and whether the results can be generalized. Therefore, we evaluated these 7 SNPs in two populations recruited from Johns Hopkins Hospital, including European Americans (EA) (1,563 cases and 576 controls) and AA (364 cases and 353 controls). Each of the previously reported risk alleles of these 7 SNPs were more common in cases than in controls among EA and AA. The differences were highly significant in EA (P = 10−4) and marginally significant in AA (P = 0.04) for 17q12SNPs. In contrast, the differences were not statistically significant in EA or AA for SNPs at 17q24.3, but were marginally significant for two SNPs (P = 0.04 - 0.06) when subjects from EA and AA were combined. Similar results were obtained for genotype and haplotype frequencies. These risk variants were not associated with aggressiveness of prostate cancer or other clinical variables such as TNM stage, pre-operative PSA, or age at diagnosis. Our results provide the first confirmation of these novel prostate loci and the first demonstration that these two loci may also play roles in prostate cancer risk among AA.

Published
2008

47. Large-scale fine mapping of the HNF1B locus and prostate cancer risk

Author

Berndt, Sonja I, Sampson, Joshua, Yeager, Meredith, Jacobs, Kevin B, Wang, Zhaoming, Hutchinson, Amy, Chung, Charles, Orr, Nick, Wacholder, Sholom, Chatterjee, Nilanjan, Yu, Kai, Kraft, Peter, Feigelson, Heather Spencer, Thun, Michael J, Diver, W Ryan, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Schumacher, Fredrick R, Cancel-Tassin, Geraldine, Cussenot, Olivier, Valeri, Antoine, Andriole, Gerald L, Crawford, E David, Haiman, Christopher, Henderson, Brian, Kolonel, Laurence, Le Marchand, Loic, Siddiq, Afshan, Riboli, Elio, Travis, Ruth C, Kaaks, Rudolf, Isaacs, William, Isaacs, Sarah, Wiley, Kathleen E, Gronberg, Henrik, Wiklund, Fredrik, Stattin, Pär, Xu, Jianfeng, Zheng, S Lilly, Sun, Jielin, Vatten, Lars J, Hveem, Kristian, Njølstad, Inger, Gerhard, Daniela S, Tucker, Margaret, Hayes, Richard B, Hoover, Robert N, Fraumeni, Joseph F, Hunter, David J, Thomas, Gilles, Chanock, Stephen J, Berndt, Sonja I, Sampson, Joshua, Yeager, Meredith, Jacobs, Kevin B, Wang, Zhaoming, Hutchinson, Amy, Chung, Charles, Orr, Nick, Wacholder, Sholom, Chatterjee, Nilanjan, Yu, Kai, Kraft, Peter, Feigelson, Heather Spencer, Thun, Michael J, Diver, W Ryan, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Schumacher, Fredrick R, Cancel-Tassin, Geraldine, Cussenot, Olivier, Valeri, Antoine, Andriole, Gerald L, Crawford, E David, Haiman, Christopher, Henderson, Brian, Kolonel, Laurence, Le Marchand, Loic, Siddiq, Afshan, Riboli, Elio, Travis, Ruth C, Kaaks, Rudolf, Isaacs, William, Isaacs, Sarah, Wiley, Kathleen E, Gronberg, Henrik, Wiklund, Fredrik, Stattin, Pär, Xu, Jianfeng, Zheng, S Lilly, Sun, Jielin, Vatten, Lars J, Hveem, Kristian, Njølstad, Inger, Gerhard, Daniela S, Tucker, Margaret, Hayes, Richard B, Hoover, Robert N, Fraumeni, Joseph F, Hunter, David J, Thomas, Gilles, and Chanock, Stephen J

Abstract

Previous genome-wide association studies have identified two independent variants in HNF1B as susceptibility loci for prostate cancer risk. To fine-map common genetic variation in this region, we genotyped 79 single nucleotide polymorphisms (SNPs) in the 17q12 region harboring HNF1B in 10 272 prostate cancer cases and 9123 controls of European ancestry from 10 case-control studies as part of the Cancer Genetic Markers of Susceptibility (CGEMS) initiative. Ten SNPs were significantly related to prostate cancer risk at a genome-wide significance level of P < 5 × 10(-8) with the most significant association with rs4430796 (P = 1.62 × 10(-24)). However, risk within this first locus was not entirely explained by rs4430796. Although modestly correlated (r(2)= 0.64), rs7405696 was also associated with risk (P = 9.35 × 10(-23)) even after adjustment for rs4430769 (P = 0.007). As expected, rs11649743 was related to prostate cancer risk (P = 3.54 × 10(-8)); however, the association within this second locus was stronger for rs4794758 (P = 4.95 × 10(-10)), which explained all of the risk observed with rs11649743 when both SNPs were included in the same model (P = 0.32 for rs11649743; P = 0.002 for rs4794758). Sequential conditional analyses indicated that five SNPs (rs4430796, rs7405696, rs4794758, rs1016990 and rs3094509) together comprise the best model for risk in this region. This study demonstrates a complex relationship between variants in the HNF1B region and prostate cancer risk. Further studies are needed to investigate the biological basis of the association of variants in 17q12 with prostate cancer.

Published
2011
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48. Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for prostate cancer Genetics using novel sumLINK and sumLOD analyses.

Author

Christensen, G Bryce, Baffoe-Bonnie, Agnes B, George, Asha, Powell, Isaac, Bailey-Wilson, Joan E, Carpten, John D, Giles, Graham G, Hopper, John L, Severi, Gianluca, English, Dallas R, Foulkes, William D, Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D, Whittemore, Alice S, Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L, Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A, Wiley, Kathleen E, Isaacs, Sarah D, Walsh, Patrick C, Isaacs, William B, Thibodeau, Stephen N, McDonnell, Shannon K, Hebbring, Scott, Schaid, Daniel J, Lange, Ethan M, Cooney, Kathleen A, Tammela, Teuvo L J, Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Grönberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Farnham, James M, Cannon-Albright, Lisa A, Camp, Nicola J, Christensen, G Bryce, Baffoe-Bonnie, Agnes B, George, Asha, Powell, Isaac, Bailey-Wilson, Joan E, Carpten, John D, Giles, Graham G, Hopper, John L, Severi, Gianluca, English, Dallas R, Foulkes, William D, Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D, Whittemore, Alice S, Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L, Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A, Wiley, Kathleen E, Isaacs, Sarah D, Walsh, Patrick C, Isaacs, William B, Thibodeau, Stephen N, McDonnell, Shannon K, Hebbring, Scott, Schaid, Daniel J, Lange, Ethan M, Cooney, Kathleen A, Tammela, Teuvo L J, Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Grönberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Farnham, James M, Cannon-Albright, Lisa A, and Camp, Nicola J

Abstract

BACKGROUND: Prostate cancer (PC) is generally believed to have a strong inherited component, but the search for susceptibility genes has been hindered by the effects of genetic heterogeneity. The recently developed sumLINK and sumLOD statistics are powerful tools for linkage analysis in the presence of heterogeneity. METHODS: We performed a secondary analysis of 1,233 PC pedigrees from the International Consortium for Prostate Cancer Genetics (ICPCG) using two novel statistics, the sumLINK and sumLOD. For both statistics, dominant and recessive genetic models were considered. False discovery rate (FDR) analysis was conducted to assess the effects of multiple testing. RESULTS: Our analysis identified significant linkage evidence at chromosome 22q12, confirming previous findings by the initial conventional analyses of the same ICPCG data. Twelve other regions were identified with genome-wide suggestive evidence for linkage. Seven regions (1q23, 5q11, 5q35, 6p21, 8q12, 11q13, 20p11-q11) are near loci previously identified in the initial ICPCG pooled data analysis or the subset of aggressive PC pedigrees. Three other regions (1p12, 8p23, 19q13) confirm loci reported by others, and two (2p24, 6q27) are novel susceptibility loci. FDR testing indicates that over 70% of these results are likely true positive findings. Statistical recombinant mapping narrowed regions to an average of 9 cM. CONCLUSIONS: Our results represent genomic regions with the greatest consistency of positive linkage evidence across a very large collection of high-risk PC pedigrees using new statistical tests that deal powerfully with heterogeneity. These regions are excellent candidates for further study to identify PC predisposition genes. Prostate (c) 2010 Wiley-Liss, Inc.

Published
2010
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49. Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for prostate cancer Genetics using novel sumLINK and sumLOD analyses

Author

University of Michigan ICPCG Group ; Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, University of Michigan ICPCG Group ; University of Michigan, Ann Arbor, Michigan, University of Utah ICPCG Group and Division of Genetic Epidemiology, University of Utah School of Medicine, Salt Lake City, Utah ; Division of Genetic Epidemiology, University of Utah School of Medicine, 391, Chipeta Way, Suite D, Salt Lake City, UT 84108., African American Hereditary Prostate Cancer ICPCG Group ; Fox Chase Cancer Center, Philadelphia, Pennsylvania ; National Human Genome Research Institute, NIH, Bethesda, Maryland, African American Hereditary Prostate Cancer ICPCG Group ; Fox Chase Cancer Center, Philadelphia, Pennsylvania, African American Hereditary Prostate Cancer ICPCG Group ; Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, African American Hereditary Prostate Cancer ICPCG Group ; National Human Genome Research Institute, NIH, Bethesda, Maryland, African American Hereditary Prostate Cancer ICPCG Group ; Translational Genomics Research Institute, Genetic Basis of Human Disease Research Division, Phoenix, Arizona, ACTANE Consortium ICPCG Group ; Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia, ACTANE Consortium ICPCG Group ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, The University of Melbourne, Melbourne, Australia, ACTANE Consortium ICPCG Group ; Department of Oncology, McGill University, Montreal, Quebec, Canada, ACTANE Consortium ICPCG Group ; The Norwegian Radium Hospital, Oslo, Norway, ACTANE Consortium ICPCG Group ; Institute of Cancer Research, Royal Marsden NHS Foundation Trust, Surrey, UK, ACTANE Consortium ICPCG Group ; Cancer Research UK Genetic Epidemiology Unit, Cambridge, UK, ACTANE Consortium ICPCG Group ; Division of Medical Genetics, University of Washington Medical Center, Seattle, Washington, BC/CA/HI ICPCG Group ; Department of Health Research and Policy, Stanford School of Medicine, Stanford, California ; Stanford Comprehensive Cancer Center, Stanford School of Medicine, Stanford, California, BC/CA/HI ICPCG Group ; Stanford Comprehensive Cancer Center, Stanford School of Medicine, Stanford, California, BC/CA/HI ICPCG Group ; Department of Urology and Department of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, California, Data Coordinating Center for the ICPCG and Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina, FHCRC ICPCG Group ; Fred Hutchinson Cancer Research Center, Divisions of Public Health Sciences, Seattle, Washington, FHCRC ICPCG Group ; Cancer Genetics Branch, National Institutes of Health, Bethesda, Maryland, FHCRC ICPCG Group ; Institute for Systems Biology, Seattle, Washington, Johns Hopkins University ICPCG Group and Department of Urology, Johns Hopkins Medical Institutions, Baltimore, Maryland, Mayo Clinic ICPCG Group and Mayo Clinic, Rochester, Minnesota, University of Tampere ICPCG Group, University of Tampere and Tampere University Hospital, Tampere, Finland, University of Ulm ICPCG Group ; Department of Urology, University of Ulm, Ulm, Germany, University of Ulm ICPCG Group ; Institute of Human Genetics, University of Ulm, Ulm, Germany, University of Ume?? ICPCG Group ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, University of Ume?? ICPCG Group ; Oncologic Centre, Ume?? University, Ume??, Sweden, University of Utah ICPCG Group and Division of Genetic Epidemiology, University of Utah School of Medicine, Salt Lake City, Utah, Christensen, G. Bryce, Baffoe-Bonnie, Agnes B., George, Asha, Powell, Isaac, Bailey-Wilson, Joan E., Carpten, John D., Giles, Graham G., Hopper, John L., Severi, Gianluca, English, Dallas R., Foulkes, William D., Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D., Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L., Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Isaacs, William B., Thibodeau, Stephen N., McDonnell, Shannon K., Hebbring, Scott, Schaid, Daniel J., Lange, Ethan M., Cooney, Kathleen A., Tammela, Teuvo L. J., Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Gr??nberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Farnham, James M., Cannon-Albright, Lisa A., Camp, Nicola J., University of Michigan ICPCG Group ; Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, University of Michigan ICPCG Group ; University of Michigan, Ann Arbor, Michigan, University of Utah ICPCG Group and Division of Genetic Epidemiology, University of Utah School of Medicine, Salt Lake City, Utah ; Division of Genetic Epidemiology, University of Utah School of Medicine, 391, Chipeta Way, Suite D, Salt Lake City, UT 84108., African American Hereditary Prostate Cancer ICPCG Group ; Fox Chase Cancer Center, Philadelphia, Pennsylvania ; National Human Genome Research Institute, NIH, Bethesda, Maryland, African American Hereditary Prostate Cancer ICPCG Group ; Fox Chase Cancer Center, Philadelphia, Pennsylvania, African American Hereditary Prostate Cancer ICPCG Group ; Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, African American Hereditary Prostate Cancer ICPCG Group ; National Human Genome Research Institute, NIH, Bethesda, Maryland, African American Hereditary Prostate Cancer ICPCG Group ; Translational Genomics Research Institute, Genetic Basis of Human Disease Research Division, Phoenix, Arizona, ACTANE Consortium ICPCG Group ; Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia, ACTANE Consortium ICPCG Group ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, The University of Melbourne, Melbourne, Australia, ACTANE Consortium ICPCG Group ; Department of Oncology, McGill University, Montreal, Quebec, Canada, ACTANE Consortium ICPCG Group ; The Norwegian Radium Hospital, Oslo, Norway, ACTANE Consortium ICPCG Group ; Institute of Cancer Research, Royal Marsden NHS Foundation Trust, Surrey, UK, ACTANE Consortium ICPCG Group ; Cancer Research UK Genetic Epidemiology Unit, Cambridge, UK, ACTANE Consortium ICPCG Group ; Division of Medical Genetics, University of Washington Medical Center, Seattle, Washington, BC/CA/HI ICPCG Group ; Department of Health Research and Policy, Stanford School of Medicine, Stanford, California ; Stanford Comprehensive Cancer Center, Stanford School of Medicine, Stanford, California, BC/CA/HI ICPCG Group ; Stanford Comprehensive Cancer Center, Stanford School of Medicine, Stanford, California, BC/CA/HI ICPCG Group ; Department of Urology and Department of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, California, Data Coordinating Center for the ICPCG and Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina, FHCRC ICPCG Group ; Fred Hutchinson Cancer Research Center, Divisions of Public Health Sciences, Seattle, Washington, FHCRC ICPCG Group ; Cancer Genetics Branch, National Institutes of Health, Bethesda, Maryland, FHCRC ICPCG Group ; Institute for Systems Biology, Seattle, Washington, Johns Hopkins University ICPCG Group and Department of Urology, Johns Hopkins Medical Institutions, Baltimore, Maryland, Mayo Clinic ICPCG Group and Mayo Clinic, Rochester, Minnesota, University of Tampere ICPCG Group, University of Tampere and Tampere University Hospital, Tampere, Finland, University of Ulm ICPCG Group ; Department of Urology, University of Ulm, Ulm, Germany, University of Ulm ICPCG Group ; Institute of Human Genetics, University of Ulm, Ulm, Germany, University of Ume?? ICPCG Group ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, University of Ume?? ICPCG Group ; Oncologic Centre, Ume?? University, Ume??, Sweden, University of Utah ICPCG Group and Division of Genetic Epidemiology, University of Utah School of Medicine, Salt Lake City, Utah, Christensen, G. Bryce, Baffoe-Bonnie, Agnes B., George, Asha, Powell, Isaac, Bailey-Wilson, Joan E., Carpten, John D., Giles, Graham G., Hopper, John L., Severi, Gianluca, English, Dallas R., Foulkes, William D., Maehle, Lovise, Moller, Pal, Eeles, Ros, Easton, Douglas, Badzioch, Michael D., Whittemore, Alice S., Oakley-Girvan, Ingrid, Hsieh, Chih-Lin, Dimitrov, Latchezar, Xu, Jianfeng, Stanford, Janet L., Johanneson, Bo, Deutsch, Kerry, McIntosh, Laura, Ostrander, Elaine A., Wiley, Kathleen E., Isaacs, Sarah D., Walsh, Patrick C., Isaacs, William B., Thibodeau, Stephen N., McDonnell, Shannon K., Hebbring, Scott, Schaid, Daniel J., Lange, Ethan M., Cooney, Kathleen A., Tammela, Teuvo L. J., Schleutker, Johanna, Paiss, Thomas, Maier, Christiane, Gr??nberg, Henrik, Wiklund, Fredrik, Emanuelsson, Monica, Farnham, James M., Cannon-Albright, Lisa A., and Camp, Nicola J.

Abstract

BACKGROUND Prostate cancer (PC) is generally believed to have a strong inherited component, but the search for susceptibility genes has been hindered by the effects of genetic heterogeneity. The recently developed sumLINK and sumLOD statistics are powerful tools for linkage analysis in the presence of heterogeneity. METHODS We performed a secondary analysis of 1,233 PC pedigrees from the International Consortium for Prostate Cancer Genetics (ICPCG) using two novel statistics, the sumLINK and sumLOD. For both statistics, dominant and recessive genetic models were considered. False discovery rate (FDR) analysis was conducted to assess the effects of multiple testing. RESULTS Our analysis identified significant linkage evidence at chromosome 22q12, confirming previous findings by the initial conventional analyses of the same ICPCG data. Twelve other regions were identified with genome-wide suggestive evidence for linkage. Seven regions (1q23, 5q11, 5q35, 6p21, 8q12, 11q13, 20p11???q11) are near loci previously identified in the initial ICPCG pooled data analysis or the subset of aggressive PC pedigrees. Three other regions (1p12, 8p23, 19q13) confirm loci reported by others, and two (2p24, 6q27) are novel susceptibility loci. FDR testing indicates that over 70% of these results are likely true positive findings. Statistical recombinant mapping narrowed regions to an average of 9???cM. CONCLUSIONS Our results represent genomic regions with the greatest consistency of positive linkage evidence across a very large collection of high-risk PC pedigrees using new statistical tests that deal powerfully with heterogeneity. These regions are excellent candidates for further study to identify PC predisposition genes. Prostate 70: 735???744, 2010. ?? 2010 Wiley-Liss, Inc.

Published
2010

50. A novel prostate cancer susceptibility locus at 19q13.

Author

Hsu, Fang-Chi, Sun, Jielin, Wiklund, Fredrik, Isaacs, Sarah D, Wiley, Kathleen E, Purcell, Lina D, Gao, Zhengrong, Stattin, Pär, Zhu, Yi, Kim, Seong-Tae, Zhang, Zheng, Liu, Wennuan, Chang, Bao-Li, Walsh, Patrick C, Duggan, David, Carpten, John D, Isaacs, William B, Grönberg, Henrik, Xu, Jianfeng, Zheng, S Lilly, Hsu, Fang-Chi, Sun, Jielin, Wiklund, Fredrik, Isaacs, Sarah D, Wiley, Kathleen E, Purcell, Lina D, Gao, Zhengrong, Stattin, Pär, Zhu, Yi, Kim, Seong-Tae, Zhang, Zheng, Liu, Wennuan, Chang, Bao-Li, Walsh, Patrick C, Duggan, David, Carpten, John D, Isaacs, William B, Grönberg, Henrik, Xu, Jianfeng, and Zheng, S Lilly

Abstract

A two-stage genome-wide association study (GWAS) of the Cancer Genetic Markers of Susceptibility (CGEMS) initiative identified single nucleotide polymorphisms (SNP) in 150 regions across the genome that may be associated with prostate cancer (PCa) risk. We filtered these results to identify 43 independent SNPs where the frequency of the risk allele was consistently higher in cases than in controls in each of the five CGEMS study populations. Genotype information for 22 of these 43 SNPs was obtained either directly by genotyping or indirectly by imputation in our PCa GWAS of 500 cases and 500 controls selected from a population-based case-control study in Sweden [Cancer of the Prostate in Sweden (CAPS)]. Two of these 22 SNPs were significantly associated with PCa risk (P<0.05). We then genotyped these two SNPs in the remaining cases (n=2,393) and controls (n=1,222) from CAPS and found that rs887391 at 19q13 was highly associated with PCa risk (P=9.4 x 10(-4)). A similar trend of association was found for this SNP in a case-control study from Johns Hopkins Hospital (JHH), albeit the result was not statistically significant. Altogether, the frequency of the risk allele of rs887391 was consistently higher in cases than controls among each of seven study populations examined, with an overall P=3.2 x 10(-7) from a combined allelic test. A fine-mapping study in a 110-kb region at 19q13 among CAPS and JHH study populations revealed that rs887391 was the most strongly associated SNP in the region. Additional confirmation studies of this region are warranted.

Published
2009
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