RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1)

J Cell Biochem. 2010 Aug 1;110(5):1039-45. doi: 10.1002/jcb.22596.

Abstract

The core binding factor (CBF) acute myeloid leukemias (AMLs) are a prognostically distinct subgroup that includes patients with the inv(16) and t(8:21) chromosomal rearrangements. Both of these rearrangements result in the formation of fusion proteins, CBFB-MYH11 and AML1-ETO, respectively, that involve members of the CBF family of transcription factors. It has been proposed that both of these fusion proteins function primarily by dominantly repressing normal CBF transcription. However, recent reports have indicted that additional, CBF-repression independent activities may be equally important during leukemogenesis. This article will focus on these recent advances.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Acute Disease
  • Core Binding Factor Alpha 2 Subunit / genetics*
  • Gene Expression Regulation, Leukemic
  • Humans
  • Leukemia / genetics*
  • Leukemia, Myeloid / genetics
  • Models, Genetic
  • Oncogene Proteins, Fusion / genetics*
  • RUNX1 Translocation Partner 1 Protein

Substances

  • AML1-ETO fusion protein, human
  • CBFbeta-MYH11 fusion protein
  • Core Binding Factor Alpha 2 Subunit
  • Oncogene Proteins, Fusion
  • RUNX1 Translocation Partner 1 Protein
  • RUNX1 protein, human