Mutation or aberrant expression of HDAC9 has been implicated in diverse conditions including ischemic stroke, schizophrenia and obesity, and also as a maker of poor outcome in cancer. HDAC9, which is subject to complex regulation via differential promoter usage and alternative splicing, is preferentially expressed in the lymphoid lineage within the hematopoietic system. HDAC9 is highly expressed in B-lymphoproliferative disorders, B-cell non-Hodgkin lymphoma cell lines and patient samples, suggesting its deregulation may lead to abnormal B-cell proliferation. These findings are supported by the recurrent amplification of the HDAC9 locus (ch 7p21.1) in B-NHL. Additionally, a number of HDAC inhibitors have been shown to possess activity in B-non-Hodgkin lymphoma. Although several in vivo mouse models examining the biological functions of the class I and II histone deacetylases are available a role for HDAC9 or other family members in B-non-Hodgkin lymphoma has not been examined in vivo.
Gil V S, et al. Deregulated expression of HDAC9 in B cells promotes development of lymphoproliferative disease and lymphoma in mice[J]. Disease Models & Mechanisms, 2016, 9(12): 1483-1495.