Search

Your search keyword '"Isaacs Sarah D"' showing total 13 results
Start Over Author "Isaacs Sarah D" Journal human genetics
13 results on '"Isaacs Sarah D"'

1. 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
Full Text
View/download PDF

2. 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
Full Text
View/download PDF

3. 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
Full Text
View/download PDF

4. 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
Full Text
View/download PDF

5. 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
Full Text
View/download PDF

9. Linkage of prostate cancer susceptibility loci to chromosome 1

Author

Xu, Jianfeng, Zheng, Siqun L., Chang, Bao-li, Smith, Jeffrey R., Carpten, John D., Stine, O. Colin, Isaacs, Sarah D., Wiley, Kathy E., Henning, Lauren, Ewing, Charles, Bujnovszky, Piroska, Bleeker, Eugene R., Walsh, Patrick C., Trent, Jeffrey M., Meyers, Deborah A., and Isaacs, William B.

Published
2001
Full Text
View/download PDF

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

Author

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

Published
2005
Full Text
View/download PDF

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

Author

Bao-Li Chang, 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, and Gronberg, Henrik

Subjects
GENETIC research, PROSTATE cancer, GENOMES, DISEASE susceptibility, GENES, CARCINOGENESIS, CELLS, HUMAN genetics, UNIVERSITIES & colleges
Abstract

Prostate cancer represents a significant worldwide public health burden. Epidemiological and genetic epidemiological studies have consistently provided data supporting the existence of inherited prostate cancer susceptibility genes. Segregation analyses of prostate cancer suggest that a multigene model may best explain familial clustering of this disease. Therefore, modeling gene–gene interactions in linkage analysis may improve the power to detect chromosomal regions harboring these disease susceptibility genes. In this study, we systematically screened for prostate cancer linkage by modeling two-locus gene–gene interactions for all possible pairs of loci across the genome in 426 prostate cancer families from Johns Hopkins Hospital, University of Michigan, University of Umeå, and University of Tampere. We found suggestive evidence for an epistatic interaction for six sets of loci (target chromosome-wide/reference marker-specific P≤0.0001). Evidence for these interactions was found in two independent subsets from within the 426 families. While the validity of these results requires confirmation from independent studies and the identification of the specific genes underlying this linkage evidence, our approach of systematically assessing gene–gene interactions across the entire genome represents a promising alternative approach for gene identification for prostate cancer. [ABSTRACT FROM AUTHOR]

Published
2006
Full Text
View/download PDF

12. Linkage of prostate cancer susceptibility loci to chromosome 1.

Author

Jianfeng Xu, Zheng, Siqun L., Bao-li Chang, Smith, Jeffrey R., Carpten, John D., Stine, O. Colin, Isaacs, Sarah D., Wiley, Kathy E., Henning, Lauren, Ewing, Charles, Bujnovszky, Piroska, Bleeker, Eugene R., Walsh, Patrick C., Trent, Jeffrey M., Meyers, Deborah A., and Isaacs, William B.

Subjects
PROSTATE cancer, ONCOGENES, DISEASE susceptibility, CHROMOSOMES, HUMAN genetics, GENETICS
Abstract

Three prostate cancer susceptibility genes have been reported to be linked to different regions on chromosome 1: HPC1 at 1q24–25, PCAP at 1q42–43, and CAPB at 1p36. Replication studies analyzing each of these regions have yielded inconsistent results. To evaluate linkage across this chromosome systematically, we performed multipoint linkage analyses with 50 microsatellite markers spanning chromosome 1 in 159 hereditary prostate cancer families (HPC), including 79 families analyzed in the original report describing HPC1 linkage. The highest lod scores for the complete dataset of 159 families were observed at 1q24–25 at which the parametric lod score assuming heterogeneity (hlod) was 2.54 (P=0.0006) with an allele sharing lod of 2.34 (P=0.001) at marker D1S413, although only weak evidence was observed in the 80 families not previously analyzed for this region (hlod=0.44, P=0.14, and allele sharing lod=0.67, P=0.08). In the complete data set, the evidence for linkage across this region was very broad, with allele sharing lod scores greater than 0.5 extending approximately 100 cM from 1p13 to 1q32, possibly indicating the presence of multiple susceptibility genes. Elsewhere on chromosome 1, some evidence of linkage was observed at 1q42–43, with a peak allele sharing lod of 0.56 (P=0.11) and hlod of 0.24 (P=0.25) at D1S235. For analysis of the CAPB locus at 1p36, we focused on six HPC families in our collection with a history of primary brain cancer; four of these families had positive linkage results at 1p36, with a peak allele sharing lod of 0.61 (P=0.09) and hlod of 0.39 (P=0.16) at D1S407 in all six families. These results are consistent with the heterogeneous nature of hereditary prostate cancer, and the existence of multiple loci on chromosome 1 for this disease. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

13. Pooled genome linkage scan of aggressive prostate cancer: results from the International Consortium for Prostate Cancer Genetics.

Author

Schaid DJ, McDonnell SK, Zarfas KE, Cunningham JM, Hebbring S, Thibodeau SN, Eeles RA, Easton DF, Foulkes WD, Simard J, Giles GG, Hopper JL, Mahle L, Moller P, Badzioch M, Bishop DT, Evans C, Edwards S, Meitz J, Bullock S, Hope Q, Guy M, Hsieh CL, Halpern J, Balise RR, Oakley-Girvan I, Whittemore AS, Xu J, Dimitrov L, Chang BL, Adams TS, Turner AR, Meyers DA, Friedrichsen DM, Deutsch K, Kolb S, Janer M, Hood L, Ostrander EA, Stanford JL, Ewing CM, Gielzak M, Isaacs SD, Walsh PC, Wiley KE, Isaacs WB, Lange EM, Ho LA, Beebe-Dimmer JL, Wood DP, Cooney KA, Seminara D, Ikonen T, Baffoe-Bonnie A, Fredriksson H, Matikainen MP, Tammela TL, Bailey-Wilson J, Schleutker J, Maier C, Herkommer K, Hoegel JJ, Vogel W, Paiss T, Wiklund F, Emanuelsson M, Stenman E, Jonsson BA, Grönberg H, Camp NJ, Farnham J, Cannon-Albright LA, Catalona WJ, Suarez BK, and Roehl KA

Subjects
Black or African American genetics, Aged, Chromosome Mapping, Family Health, Female, Genetic Heterogeneity, Genetic Predisposition to Disease ethnology, Genotype, Humans, International Cooperation, Lod Score, Male, Microsatellite Repeats, Middle Aged, Pedigree, Prostatic Neoplasms ethnology, White People genetics, Genetic Linkage, Genome, Human, Prostatic Neoplasms genetics
Abstract

While it is widely appreciated that prostate cancers vary substantially in their propensity to progress to a life-threatening stage, the molecular events responsible for this progression have not been identified. Understanding these molecular mechanisms could provide important prognostic information relevant to more effective clinical management of this heterogeneous cancer. Hence, through genetic linkage analyses, we examined the hypothesis that the tendency to develop aggressive prostate cancer may have an important genetic component. Starting with 1,233 familial prostate cancer families with genome scan data available from the International Consortium for Prostate Cancer Genetics, we selected those that had at least three members with the phenotype of clinically aggressive prostate cancer, as defined by either high tumor grade and/or stage, resulting in 166 pedigrees (13%). Genome-wide linkage data were then pooled to perform a combined linkage analysis for these families. Linkage signals reaching a suggestive level of significance were found on chromosomes 6p22.3 (LOD = 3.0), 11q14.1-14.3 (LOD = 2.4), and 20p11.21-q11.21 (LOD = 2.5). For chromosome 11, stronger evidence of linkage (LOD = 3.3) was observed among pedigrees with an average at diagnosis of 65 years or younger. Other chromosomes that showed evidence for heterogeneity in linkage across strata were chromosome 7, with the strongest linkage signal among pedigrees without male-to-male disease transmission (7q21.11, LOD = 4.1), and chromosome 21, with the strongest linkage signal among pedigrees that had African American ancestry (21q22.13-22.3; LOD = 3.2). Our findings suggest several regions that may contain genes which, when mutated, predispose men to develop a more aggressive prostate cancer phenotype. This provides a basis for attempts to identify these genes, with potential clinical utility for men with aggressive prostate cancer and their relatives.

Published
2006
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results