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 language | English (US) |
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Pages (from-to) | 66255-66266 |
Number of pages | 12 |
Journal | Oncotarget |
Volume | 7 |
Issue number | 40 |
DOIs | |
State | Published - 2016 |
Keywords
- AML
- CBFß
- CBFβ-SMMHC
- Inv(16)
- RUNX1
ASJC Scopus subject areas
- Oncology