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|Title:||Genomic analysis of marginal zone and lymphoplasmacytic lymphomas identified common and disease-specific abnormalities||Authors:||Braggio, E.
|Issue Date:||May-2012||Citation:||Braggio, E., Dogan, A., Keats, J.J., Chng, W.J., Huang, G., Matthews, J.M., Maurer, M.J., Law, M.E., Bosler, D.S., Barrett, M., Lossos, I.S., Witzig, T.E., Fonseca, R. (2012-05). Genomic analysis of marginal zone and lymphoplasmacytic lymphomas identified common and disease-specific abnormalities. Modern Pathology 25 (5) : 651-660. ScholarBank@NUS Repository. https://doi.org/10.1038/modpathol.2011.213||Abstract:||Lymphoplasmacytic lymphomas and marginal zone lymphomas of nodal, extra-nodal and splenic types account for 10% of non-Hodgkin lymphomas. They are similar at the cell differentiation level, sometimes making difficult to distinguish them from other indolent non-Hodgkin lymphomas. To better characterize their genetic basis, we performed array-based comparative genomic hybridization in 101 marginal zone lymphomas (46 MALT, 35 splenic and 20 nodal marginal zone lymphomas) and 13 lymphoplasmacytic lymphomas. Overall, 90% exhibited copy-number abnormalities. Lymphoplasmacytic lymphomas demonstrated the most complex karyotype (median=7 copy-number abnormalities), followed by MALT (4), nodal (3.5) and splenic marginal zone lymphomas (3). A comparative analysis exposed a group of copy-number abnormalities shared by several or all the entities with few disease-specific abnormalities. Gain of chromosomes 3, 12 and 18 and loss of 6q23-q24 (TNFAIP3) were identified in all entities. Losses of 13q14.3 (MIRN15A-MIRN16-1) and 17p13.3-p12 (TP53) were found in lymphoplasmacytic and splenic marginal zone lymphomas; loss of 11q21-q22 (ATM) was found in nodal, splenic marginal zone and lymphoplasmacytic lymphomas and loss of 7q32.1-q33 was found in MALT, splenic and lymphoplasmacytic lymphomas. Abnormalities affecting the nuclear factor kappa B pathway were observed in 70% of MALT and lymphoplasmacytic lymphomas and 30% of splenic and nodal marginal zone lymphomas, suggesting distinct roles of this pathway in the pathogenesis/progression of these subtypes. Elucidation of the genetic alterations contributing to the pathogenesis of these lymphomas may guide to design-specific therapeutic approaches. © 2012 USCAP, Inc. All rights reserved.||Source Title:||Modern Pathology||URI:||http://scholarbank.nus.edu.sg/handle/10635/110742||ISSN:||08933952||DOI:||10.1038/modpathol.2011.213|
|Appears in Collections:||Staff Publications|
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