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2. Evaluation of Linkage of Breast Cancer to the Putative BRCA3 Locus on Chromosome 13q21 in 128 Multiple Case Families from the Breast Cancer Linkage Consortium

Author

Thompson, Deborah, Szabo, Csilla I., Mangion, Jon, Oldenburg, Rogier A., Odefrey, Fabrice, Seal, Sheila, Barfoot, Rita, Kroeze-Jansema, Karin, Teare, Dawn, Rahman, Nazneen, Renard, Hélène, Mann, Graham, Hopper, John L., Buys, Saundra S., Andrulis, Irene L., Senie, Ruby, Daly, Mary B., West, Dee, Ostrander, Elaine A., Offit, Ken, Peretz, Tamar, Osorio, Ana, Benitez, J., Nathanson, Katherine L., Sinilnikova, Olga M., Oláh, Edith, Bignon, Yves-Jean, Ruiz, Pablo, Badzioch, Michael D., Futreal, Andrew P., Phelan, Catherine M., Narod, Steven A., Lynch, Henry T., Eeles, Ros A., Meijers-Heijboer, Hanne, Stoppa-Lyonnet, Dominique, Couch, Fergus J., Eccles, Diana M., Evans, D. Gareth, Chang-Claude, Jenny, Lenoir, Gilbert, Weber, Barbara L., Devilee, Peter, Easton, Douglas F., Goldgar, David E., and Stratton, Michael R.

Published
2002

5. 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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6. 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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7. 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

9. 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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10. Familial breast cancer risks: effects of prostate and other cancers

Author

Anderson, David E. and Badzioch, Michael D.

Subjects
Breast cancer -- Risk factors, Prostate cancer -- Genetic aspects, Endometrial cancer -- Genetic aspects, Ovarian cancer -- Genetic aspects, Cancer patients -- Family, Familial diseases -- Genetic aspects, Registries (in medicine) -- Usage, Health
Abstract

Background. Previous studies have provided conflicting results concerning the effects of a family history of prostate and other cancers on breast cancer risks. Methods. Three groups of families were studied to determine the effects of a family history of prostate cancer on breast cancer risks. Also considered were the effects of a family history of melanoma, colon, lung, ovarian, and endometrial cancers. Included were 422 first-degree female relatives of 114 patients with bilateral breast cancer, 320 first-degree relatives of 88 male patients with breast cancer, and 633 relatives of 186 unselected female patients. For estimating relative risks, observed numbers of breast cancers in relatives were compared with expected numbers based on population incidence data. Multiple logistic-regression also provided odds ratios of relatives affected with breast cancer. Results. A family history of prostate cancer increased the breast cancer risks in each of the groups, compared with families without prostate cancer. Ovarian cancer in a family increased the breast cancer risks only in the bilateral breast cancer group, and endometrial cancer increased the risks in the bilateral and unselected groups. These increases in risk appeared to be the consequence of families with multiple cancers, including those with hereditary breast-ovarian cancers and the cancer family syndrome. A family history of melanoma, lung, or colon cancer did not increase breast cancer risks. Conclusions. A family history of prostate cancer, as well as endometrial and ovarian cancer, significantly increases the risk of breast cancer.

Published
1993

11. Breast cancer risks in relatives of male breast cancer patients

Author

Anderson, David E. and Badzioch, Michael D.

Subjects
Breast cancer -- Risk factors, Cancer patients -- Family, Men -- Diseases, Health
Abstract

Background: Previous studies have provided conflicting results concerning the familial effect of male breast cancer on breast cancer risks in female relatives. Purpose: We studied breast cancer risks in first-degree relatives of male patients and compared them with relatives of female patients. Methods: Our study included 88 consecutively ascertained male patients and 320 of their first-degree relatives as well as 186 consecutively ascertained female patients and 633 of their first-degree relatives. Observed numbers of breast cancers in relatives were compared with the expected number derived from the Connecticut Tumor Registry. Multiple logistic regression analysis was also performed. Results: Relatives of male patients exhibited a significant twofold increased risk when compared with expected rates and no difference in risk when compared with that of relatives of female patients. Prostate cancer in the family of a male patient resulted in a significant fourfold increased breast cancer risk compared with a risk of 1.4 in families with no history of prostate cancer. A family history of lung cancer, colon cancer, or melanoma had no effect on increasing risks of breast cancer. Conclusion: The familial effect of male breast cancer is the same as that of female breast cancer. Implications: Any estimates of breast cancer risk provided to individuals should also consider the occurrence of prostate cancer in the family, since prostate cancer appears capable of at least doubling the underlying twofold risk. [J Natl Cancer Inst 84:1114-1117, 1992]

Published
1992

12. 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

13. 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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14. 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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15. 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

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

Published
2010
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21. Genomic scan of 254 hereditary prostate cancer families

Author

Janer, Marta, primary, Friedrichsen, Danielle M., additional, Stanford, Janet L., additional, Badzioch, Michael D., additional, Kolb, Suzanne, additional, Deutsch, Kerry, additional, Peters, Mette A., additional, Goode, Ellen L., additional, Welti, Russ, additional, DeFrance, Hawkins B., additional, Iwasaki, Lori, additional, Li, Sarah, additional, Hood, Leroy, additional, Ostrander, Elaine A., additional, and Jarvik, Gail P., additional

Published
2003
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30. A common VLDLRpolymorphism interacts with APOEgenotype in the prediction of carotid artery disease risks⃞

Author

Crawford, Dana C., Nord, Alex S., Badzioch, Michael D., Ranchalis, Jane, McKinstry, Laura A., Ahearn, Magdalena, Bertucci, Caterina, Shephard, Cynthia, Wong, Michelle, Rieder, Mark J., Schellenberg, Gerard D., Nickerson, Deborah A., Heagerty, Patrick J., Wijsman, Ellen M., and Jarvik, Gail P.

Abstract

The genetic factors associated with carotid artery disease (CAAD) are not fully known. Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLRwas resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5′ flanking region of VLDLRwas associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR1226 and APOEgenotype for predicting CAAD case status. These findings may further our understanding of VLDLR function, its ligand APOE, and ultimately the pathogenesis of CAAD in the general population.

Published
2008
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