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TFIID and MYB Share a Therapeutic Handshake in AML

Charles C Bell1, Mark A Dawson2

  • 1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, VIC 3052, Australia.

Cancer Cell
|January 10, 2018
PubMed

Insights

Targeting cancer-driving transcription factors is difficult. This study shows disrupting the MYB-TFIID interaction offers a new therapeutic strategy for acute myeloid leukemia (AML).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Targeted cancer therapies aim to disrupt specific oncogenic drivers.
  • Selectively inhibiting transcription factors has been a significant challenge in drug development.
  • Acute myeloid leukemia (AML) often involves dysregulated transcription factors.

Purpose of the Study:

  • To demonstrate a proof-of-concept for disrupting the interaction between MYB and TFIID.
  • To explore this disruption as a potential therapeutic strategy for AML.

Main Methods:

  • Investigated the interaction between the MYB transcription factor and the general transcriptional coactivator TFIID.
  • Developed and tested a method to specifically disrupt this interaction.

Main Results:

  • Successfully demonstrated that the MYB-TFIID interaction can be specifically disrupted.
  • Showcased the therapeutic potential of this disruption in AML models.

Conclusions:

  • Disrupting the MYB-TFIID interaction is a viable strategy for targeting oncogenic transcription factors.
  • This approach offers a novel therapeutic avenue for AML treatment.

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