HDAC inhibitor

HDACs’ expression is often deregulated in cancers, neurological diseases and immune disorders. The first reports about aberrant chromatin acetylation in cancer were described for a subtype of acute myeloid leukaemia with a recurrent translocation t and for acute promyelocytic leukaemia with the t translocation generating the PML-RARa protein fusion. However, there is minimal definitive experimental evidence that HDAC overexpression is oncogenic except for HDAC2 that may have a functional role in colorectal tumorigenesis. Indeed, inhibition of HDAC1, HDAC2, or HDAC3 may in certain circumstances be tumour promoting. Aberrant HDAC expression and function lead to neuropathology: learning and memory dysfunction, neurodegenerative and neurological diseases (like Alzheimer’s disease and Parkinson’s disease, respectively), neuronal development, depression and anxiety. HDACs are target for cancer treatment in leukaemia’s and myelodysplastic syndromes. Many clinical trials are ongoing for solid tumours. However clinical results have been often disappointing.