American Society of Hematology, Blood, 26(128), p. 3023-3024, 2016
DOI: 10.1182/blood-2016-11-748145
Full text: Unavailable
In this issue of Blood, Bottoni et al demonstrate that histone deacetylase (HDAC) inhibition promotes the upregulation of microRNAs (miRNAs or miRs) which target Bruton tyrosine kinase (BTK), subsequently suppressing prosurvival signaling in chronic lymphocytic leukemia (CLL) samples, and highlight a rationale for HDAC inhibitors in combination with ibrutinib to treat patients.1