Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia

Lisa Richter, Yiqian Wang, R. Katherine Hyde

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Inversion of chromosome 16 (inv(16)) generates the CBFβ-SMMHC fusion protein and is found in nearly all patients with acute myeloid leukemia subtype M4 with Eosinophilia (M4Eo). Expression of CBFβ-SMMHC is causative for leukemia development, but the molecular mechanisms underlying its activity are unclear. Recently, there have been important advances in defining the role of CBFβ-SMMHC and its binding partners, the transcription factor RUNX1 and the histone deacetylase HDAC8. Importantly, initial trials demonstrate that small molecules targeting these binding partners are effective against CBFβ-SMMHC induced leukemia. This review will discuss recent advances in defining the mechanism of CBFβ-SMMHC activity, as well as efforts to develop new therapies for inv(16) AML.

Original languageEnglish (US)
Pages (from-to)66255-66266
Number of pages12
JournalOncotarget
Volume7
Issue number40
DOIs
StatePublished - 2016

Keywords

  • AML
  • CBFß
  • CBFβ-SMMHC
  • Inv(16)
  • RUNX1

ASJC Scopus subject areas

  • Oncology

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