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Histone deacetylases ( HDAC s) critically regulate gene expression by determining the acetylation status of histones. Studies have increasingly focused on the activities of  HDAC s, especially involving non‐histone proteins, and their various biological effects. Aberrant  HDAC  expression observed in several kinds of human tumors makes  HDAC s potential targets for cancer treatment. Several preclinical studies have suggested that  HDAC  inhibitors show some efficacy in the treatment of acute myelogenous leukemia with  AML 1‐ ETO , which mediates transcriptional repression through its interaction with a complex including  HDAC 1. Recurrent mutations in epigenetic regulators are found in T‐cell lymphomas ( TCL s), and  HDAC  inhibitors and hypomethylating agents were shown to act cooperatively in the treatment of  TCL s. Preclinical modeling has suggested that persistent activation of the signal transducer and activator of transcription signaling pathway could serve as a useful biomarker of resistance to  HDAC  inhibitor in patients with cutaneous  TCL . Panobinostat, a pan‐ HDAC  inhibitor, in combination with bortezomib and dexamethasone, has achieved longer progression‐free survival in patients with relapsed/refractory multiple myeloma ( MM ) than the placebo in combination with bortezomib and dexamethasone. Panobinostat inhibited  MM  cell growth by degrading protein phosphatase 3 catalytic subunit α ( PPP 3 CA ), a catalytic subunit of calcineurin. This degradation was suggested to be mediated by the blockade of the chaperone function of heat shock protein 90 due to  HDAC 6 inhibition. Aberrant   PPP 3 CA   expression in advanced  MM  indicated a possible correlation between high   PPP 3 CA   expression and the pathogenesis of  MM . Furthermore,  PPP 3 CA  was suggested as a common target of panobinostat and bortezomib.

Action mechanisms of histone deacetylase inhibitors in the treatment of hematological malignancies