
Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat
Author(s) -
Tiewei Cheng,
Kendall J. Kiser,
Leslie Grasse,
LaKesla R. Iles,
Geoffrey Bartholomeusz,
Felipe Samaniego,
Robert Z. Orłowski,
Joya Chandra
Publication year - 2021
Publication title -
cancer drug resistance (alhambra, calif.)
Language(s) - English
Resource type - Journals
eISSN - 2578-532X
DOI - 10.20517/cdr.2021.44
Subject(s) - panobinostat , drug resistance , bortezomib , histone deacetylase , drug , histone deacetylase inhibitor , medicine , cancer research , multiple myeloma , histone , pharmacology , oncology , biology , gene , genetics
Multiple myeloma (MM) is a hematological malignancy of antibody-producing mature B cells or plasma cells. The proteasome inhibitor, bortezomib, was the first-in-class compound to be FDA approved for MM and is frequently utilized in induction therapy. However, bortezomib refractory disease is a major clinical concern, and the efficacy of the pan-histone deacetylase inhibitor (HDACi), panobinostat, in bortezomib refractory disease indicates that HDAC targeting is a viable strategy. Here, we utilized isogenic bortezomib resistant models to profile HDAC expression and define baseline and HDACi-induced expression patterns of individual HDAC family members in sensitive vs. resistant cells to better understanding the potential for targeting these enzymes.