Frontiers of Medicine

, Volume 6, Issue 3, pp 248–262

AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches


DOI: 10.1007/s11684-012-0206-6

Cite this article as:
Hatlen, M.A., Wang, L. & Nimer, S.D. Front. Med. (2012) 6: 248. doi:10.1007/s11684-012-0206-6


The AML1-ETO fusion transcription factor is generated by the t(8;21) translocation, which is present in approximately 4%–12% of adult and 12%–30% of pediatric acute myeloid leukemia (AML) patients. Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events. In this review, we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo. We also discuss potential therapeutic strategies for t(8;21) positive AML that involve targeting the fusion protein itself, the proteins that bind to it, or the genes that it regulates. Recently published studies suggest that a targeted therapy for t(8;21) positive AML is feasible and may be coming sometime soon.


AML1-ETO mouse model leukemia t(8;21) pathway hits mutation hematopoiesis Kasumi-1 CD34+ 

Copyright information

© Higher Education Press and Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • Megan A. Hatlen
    • 1
    • 2
  • Lan Wang
    • 1
  • Stephen D. Nimer
    • 1
    • 2
  1. 1.Molecular Pharmacology and Chemistry ProgramSloan-Kettering Institute, Memorial Sloan-Kettering Cancer CenterNew YorkUSA
  2. 2.Weill Cornell Medical CollegeNew YorkUSA

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