Inhibition of bromodomain and extra-terminal proteins increases sensitivity to venetoclax in chronic lymphocytic leukaemia

J Cell Mol Med. 2020 Jan;24(2):1650-1657. doi: 10.1111/jcmm.14857. Epub 2019 Dec 10.

Abstract

The development of drugs able to target BTK, PI3k-delta and BCL2 has dramatically improved chronic lymphocytic leukaemia (CLL) therapies. However, drug resistance to these therapies has already been reported due to non-recurrent changes in oncogenic pathways and genes expression signatures. In this study, we investigated the cooperative role of the BCL2 inhibitor venetoclax and the BRD4 inhibitor JQ1. In particular, we found that JQ1 shows additional activity with venetoclax, in CLL cell lines and in ex vivo isolated primary CD19+ lymphocytes, arguing in favour of combination strategies. Lastly, JQ1 is also effective in venetoclax-resistant CLL cell lines. Together, our findings indicated that the BET inhibitor JQ1 could be a promising therapy in CLL, both as first-line therapy in combination with venetoclax and as second-line therapy, after the emergence of venetoclax-resistant clones.

Keywords: BCL-2; BET inhibitor; BRD4; chronic lymphocytic leukaemia; venetoclax.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Azepines / pharmacology
  • Bridged Bicyclo Compounds, Heterocyclic / pharmacology
  • Bridged Bicyclo Compounds, Heterocyclic / therapeutic use*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Drug Synergism
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy*
  • Sulfonamides / pharmacology
  • Sulfonamides / therapeutic use*
  • Transcription Factors / antagonists & inhibitors*
  • Transcription Factors / metabolism
  • Triazoles / pharmacology

Substances

  • (+)-JQ1 compound
  • Azepines
  • Bridged Bicyclo Compounds, Heterocyclic
  • Sulfonamides
  • Transcription Factors
  • Triazoles
  • venetoclax