_version_ 1836399091216547840
autor Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
beschreibung The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG- MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG- MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.
citation_standardnr 6360045
datenlieferant ipn_articles
feed_id 310
feed_publisher American Society of Hematology (ASH)
feed_publisher_url http://www.hematology.org/
insertion_date 2018-11-23
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/132/21/2280?rss=1
schlagwort Lymphoid Neoplasia, Brief Reports
search_space articles
shingle_author_1 Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
shingle_author_2 Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
shingle_author_3 Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
shingle_author_4 Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
shingle_catch_all_1 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
Lymphoid Neoplasia, Brief Reports
The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG- MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG- MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.
Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
American Society of Hematology (ASH)
0006-4971
00064971
1528-0020
15280020
shingle_catch_all_2 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
Lymphoid Neoplasia, Brief Reports
The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG- MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG- MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.
Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
American Society of Hematology (ASH)
0006-4971
00064971
1528-0020
15280020
shingle_catch_all_3 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
Lymphoid Neoplasia, Brief Reports
The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG- MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG- MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.
Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
American Society of Hematology (ASH)
0006-4971
00064971
1528-0020
15280020
shingle_catch_all_4 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
Lymphoid Neoplasia, Brief Reports
The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG- MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG- MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.
Wagener, R., Lopez, C., Kleinheinz, K., Bausinger, J., Aukema, S. M., Nagel, I., Toprak, U. H., Seufert, J., Altmüller, J., Thiele, H., Schneider, C., Kolarova, J., Park, J., Hübschmann, D., Murga Penas, E. M., Drexler, H. G., Attarbaschi, A., Hovland, R., Kjeldsen, E., Kneba, M., Kontny, U., de Leval, L., Nürnberg, P., Oschlies, I., Oscier, D., Schlegelberger, B., Stilgenbauer, S., Wössmann, W., Schlesner, M., Burkhardt, B., Klapper, W., Jaffe, E. S., Küppers, R., Siebert, R.
American Society of Hematology (ASH)
0006-4971
00064971
1528-0020
15280020
shingle_title_1 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
shingle_title_2 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
shingle_title_3 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
shingle_title_4 IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
timestamp 2025-06-30T23:37:27.176Z
titel IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
titel_suche IG-MYC+ neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas
topic W
WW-YZ
uid ipn_articles_6360045