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Updated: Dec 1, 2025

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
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Bromodomain and extra-terminal (BET) inhibitors in treating myeloid neoplasms

Natalie Cheng Chen1, Gautam Borthakur2, Naveen Pemmaraju2

  • 1Department of Internal Medicine, The University of Texas School of Health Sciences at Houston, Houston, TX, USA.

Leukemia & Lymphoma
|November 9, 2020
PubMed

Insights

Bromodomain extra-terminal inhibitors (BETi) show promise for treating myeloid neoplasms. Research reviews preclinical and clinical data on BETi

Area of Science:

  • Oncology
  • Epigenetics
  • Pharmacology

Background:

  • Cancer development involves epigenetic alterations.
  • Novel agents targeting epigenetic pathways, such as bromodomain inhibitors, are under investigation.
  • Bromodomain and extra-terminal inhibitors (BETi) are a class of agents targeting epigenetic modifications.

Purpose of the Study:

  • To discuss epigenetic modulation focusing on BET inhibitors in myeloid neoplasms.
  • To review and summarize preclinical and clinical data on BETi in treating myeloid neoplasms.

Main Methods:

  • Comprehensive literature review of preclinical studies.
  • Systematic review of early clinical trials.
  • Analysis of data on BETi efficacy and safety in myeloid neoplasms.

Main Results:

  • Approximately 20 BET inhibitors have been developed.
  • Preclinical and early clinical studies suggest BETi activity in hematological malignancies.
  • Emerging data indicates potential for BETi in treating acute myeloid leukemia, blastic plasmacytoid dendritic cell neoplasm, myeloproliferative neoplasms, and lymphoma.

Conclusions:

  • BET inhibitors represent a promising therapeutic strategy for myeloid neoplasms.
  • Further clinical investigation is warranted to establish the role of BETi in managing these diseases.
  • Epigenetic modulation with BETi offers a novel approach to cancer treatment.
Keywords:
BET inhibitorsCancerepigeneticsmyeloid neoplasm

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