Bcl-2 inhibition or FBXW7 mutation sensitizes solid tumor cells to HDAC inhibition in vitro but could prove difficult to validate in patients

Abstract

In this issue of Cancer Discovery, He and colleagues determined that Mcl-1 levels are a key factor in the response to histone deacetylase (HDAC) inhibitors, and FBXW7 mutation is a biomarker for sensitivity to HDAC inhibition. They also present evidence for synergy between treatment with HDAC inhibitors and Bcl-2-targeted therapeutics. These data provide an exciting new biomarker and combination therapy that should be evaluated clinically.