Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma
Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S.
American Society of Hematology (ASH)
Published 2018
American Society of Hematology (ASH)
Published 2018
Publication Date: |
2018-11-09
|
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Publisher: |
American Society of Hematology (ASH)
|
Print ISSN: |
0006-4971
|
Electronic ISSN: |
1528-0020
|
Topics: |
Biology
Medicine
|
Keywords: |
Immunobiology and Immunotherapy, Lymphoid Neoplasia
|
Published by: |
_version_ | 1839208224428916736 |
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autor | Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. |
beschreibung | To further our understanding of inherited susceptibility to Hodgkin lymphoma (HL), we performed a meta-analysis of 7 genome-wide association studies totaling 5325 HL cases and 22 423 control patients. We identify 5 new HL risk loci at 6p21.31 (rs649775; P = 2.11 x 10 –10 ), 6q23.3 (rs1002658; P = 2.97 x 10 –8 ), 11q23.1 (rs7111520; P = 1.44 x 10 –11 ), 16p11.2 (rs6565176; P = 4.00 x 10 –8 ), and 20q13.12 (rs2425752; P = 2.01 x 10 –8 ). Integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the 5 new and 13 known risk loci implicates dysfunction of the germinal center reaction, disrupted T-cell differentiation and function, and constitutive NF-B activation as mechanisms of predisposition. These data provide further insights into the genetic susceptibility and biology of HL. |
citation_standardnr | 6354989 |
datenlieferant | ipn_articles |
feed_id | 310 |
feed_publisher | American Society of Hematology (ASH) |
feed_publisher_url | http://www.hematology.org/ |
insertion_date | 2018-11-09 |
journaleissn | 1528-0020 |
journalissn | 0006-4971 |
publikationsjahr_anzeige | 2018 |
publikationsjahr_facette | 2018 |
publikationsjahr_intervall | 7984:2015-2019 |
publikationsjahr_sort | 2018 |
publisher | American Society of Hematology (ASH) |
quelle | Blood |
relation | http://www.bloodjournal.org/cgi/content/short/132/19/2040?rss=1 |
schlagwort | Immunobiology and Immunotherapy, Lymphoid Neoplasia |
search_space | articles |
shingle_author_1 | Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. |
shingle_author_2 | Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. |
shingle_author_3 | Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. |
shingle_author_4 | Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. |
shingle_catch_all_1 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma Immunobiology and Immunotherapy, Lymphoid Neoplasia To further our understanding of inherited susceptibility to Hodgkin lymphoma (HL), we performed a meta-analysis of 7 genome-wide association studies totaling 5325 HL cases and 22 423 control patients. We identify 5 new HL risk loci at 6p21.31 (rs649775; P = 2.11 x 10 –10 ), 6q23.3 (rs1002658; P = 2.97 x 10 –8 ), 11q23.1 (rs7111520; P = 1.44 x 10 –11 ), 16p11.2 (rs6565176; P = 4.00 x 10 –8 ), and 20q13.12 (rs2425752; P = 2.01 x 10 –8 ). Integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the 5 new and 13 known risk loci implicates dysfunction of the germinal center reaction, disrupted T-cell differentiation and function, and constitutive NF-B activation as mechanisms of predisposition. These data provide further insights into the genetic susceptibility and biology of HL. Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. American Society of Hematology (ASH) 0006-4971 00064971 1528-0020 15280020 |
shingle_catch_all_2 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma Immunobiology and Immunotherapy, Lymphoid Neoplasia To further our understanding of inherited susceptibility to Hodgkin lymphoma (HL), we performed a meta-analysis of 7 genome-wide association studies totaling 5325 HL cases and 22 423 control patients. We identify 5 new HL risk loci at 6p21.31 (rs649775; P = 2.11 x 10 –10 ), 6q23.3 (rs1002658; P = 2.97 x 10 –8 ), 11q23.1 (rs7111520; P = 1.44 x 10 –11 ), 16p11.2 (rs6565176; P = 4.00 x 10 –8 ), and 20q13.12 (rs2425752; P = 2.01 x 10 –8 ). Integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the 5 new and 13 known risk loci implicates dysfunction of the germinal center reaction, disrupted T-cell differentiation and function, and constitutive NF-B activation as mechanisms of predisposition. These data provide further insights into the genetic susceptibility and biology of HL. Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. American Society of Hematology (ASH) 0006-4971 00064971 1528-0020 15280020 |
shingle_catch_all_3 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma Immunobiology and Immunotherapy, Lymphoid Neoplasia To further our understanding of inherited susceptibility to Hodgkin lymphoma (HL), we performed a meta-analysis of 7 genome-wide association studies totaling 5325 HL cases and 22 423 control patients. We identify 5 new HL risk loci at 6p21.31 (rs649775; P = 2.11 x 10 –10 ), 6q23.3 (rs1002658; P = 2.97 x 10 –8 ), 11q23.1 (rs7111520; P = 1.44 x 10 –11 ), 16p11.2 (rs6565176; P = 4.00 x 10 –8 ), and 20q13.12 (rs2425752; P = 2.01 x 10 –8 ). Integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the 5 new and 13 known risk loci implicates dysfunction of the germinal center reaction, disrupted T-cell differentiation and function, and constitutive NF-B activation as mechanisms of predisposition. These data provide further insights into the genetic susceptibility and biology of HL. Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. American Society of Hematology (ASH) 0006-4971 00064971 1528-0020 15280020 |
shingle_catch_all_4 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma Immunobiology and Immunotherapy, Lymphoid Neoplasia To further our understanding of inherited susceptibility to Hodgkin lymphoma (HL), we performed a meta-analysis of 7 genome-wide association studies totaling 5325 HL cases and 22 423 control patients. We identify 5 new HL risk loci at 6p21.31 (rs649775; P = 2.11 x 10 –10 ), 6q23.3 (rs1002658; P = 2.97 x 10 –8 ), 11q23.1 (rs7111520; P = 1.44 x 10 –11 ), 16p11.2 (rs6565176; P = 4.00 x 10 –8 ), and 20q13.12 (rs2425752; P = 2.01 x 10 –8 ). Integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the 5 new and 13 known risk loci implicates dysfunction of the germinal center reaction, disrupted T-cell differentiation and function, and constitutive NF-B activation as mechanisms of predisposition. These data provide further insights into the genetic susceptibility and biology of HL. Sud, A., Thomsen, H., Orlando, G., Försti, A., Law, P. J., Broderick, P., Cooke, R., Hariri, F., Pastinen, T., Easton, D. F., Pharoah, P. D. P., Dunning, A. M., Peto, J., Canzian, F., Eeles, R., Kote-Jarai, Z., Muir, K., Pashayan, N., Campa, D., the PRACTICAL Consortium, Hoffmann, P., Nöthen, M. M., Jöckel, K.-H., von Strandmann, E. P., Swerdlow, A. J., Engert, A., Orr, N., Hemminki, K., Houlston, R. S. American Society of Hematology (ASH) 0006-4971 00064971 1528-0020 15280020 |
shingle_title_1 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
shingle_title_2 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
shingle_title_3 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
shingle_title_4 | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
timestamp | 2025-07-31T23:47:25.782Z |
titel | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
titel_suche | Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma |
topic | W WW-YZ |
uid | ipn_articles_6354989 |