{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T02:49:01Z","timestamp":1787021341849,"version":"build-2736575974"},"reference-count":83,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2021,5,18]],"date-time":"2021-05-18T00:00:00Z","timestamp":1621296000000},"content-version":"am","delay-in-days":1964,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0"}],"funder":[{"DOI":"10.13039\/501100000391","name":"Association for International Cancer Research","doi-asserted-by":"publisher","award":["11-0301"],"award-info":[{"award-number":["11-0301"]}],"id":[{"id":"10.13039\/501100000391","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000289","name":"Cancer Research UK","doi-asserted-by":"crossref","award":["A12747"],"award-info":[{"award-number":["A12747"]}],"id":[{"id":"10.13039\/501100000289","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000651","name":"Leukaemia and Lymphoma Research","doi-asserted-by":"publisher","award":["11046"],"award-info":[{"award-number":["11046"]}],"id":[{"id":"10.13039\/501100000651","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>Histone Deacetylase 9 (HDAC9) is expressed in B-cells and its overexpression has been observed in B-lymphoproliferative disorders and B-cell non-Hodgkin lymphomas (B-NHL). We examined HDAC9 protein expression and copy number alterations in primary B-NHL samples, identifying high HDAC9 expression among various lymphoma entities and HDAC9 copy number gains in 50% of diffuse large B-cell lymphoma (DLBCL). To study the role of HDAC9 in lymphomagenesis we generated a genetically engineered mouse (GEM) model that constitutively expressed an HDAC9 transgene throughout B-cell development under the control of the immunoglobulin heavy chain (IgH) enhancer (E\u03bc). Here we report that the E\u03bc-HDAC9 GEM model developed splenic marginal zone lymphoma and lymphoproliferative disease (LPD) with progression towards aggressive DLBCL, with gene expression profiling supporting a germinal centre cell origin in common with human tumors. Analysis of E\u03bc-HDAC9 tumors suggested that HDAC9 may contribute to lymphomagenesis by altering pathways involved in growth and survival as well as modulating BCL6 activity and p53 tumor suppressor function. Epigenetic modifications play an important role in the germinal center response and deregulation of the B-cell epigenome as a consequence of mutations and other genomic aberrations are being increasingly recognized as important steps in the pathogenesis of a variety of B- cell lymphomas. A thorough mechanistic understanding of these alterations will inform the use of targeted therapies for these malignancies. These findings strongly suggest a role for HDAC9 in B-NHL and establish a novel GEM model for the study of lymphomagenesis and, potentially, pre-clinical testing of therapeutic approaches based on histone deacetylase inhibitors.<\/jats:p>","DOI":"10.1242\/dmm.023366","type":"journal-article","created":{"date-parts":[[2016,10,28]],"date-time":"2016-10-28T20:40:32Z","timestamp":1477687232000},"source":"Crossref","is-referenced-by-count":22,"title":["Deregulated expression of HDAC9 in B-cells promotes development of lymphoproliferative disease and lymphoma"],"prefix":"10.1242","author":[{"given":"V. 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