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

Megan A. Hatlen, Lan Wang, Stephen D. Nimer

Research output: Contribution to journalReview articlepeer-review

53 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)248-262
Number of pages15
JournalFrontiers of Medicine in China
Issue number3
StatePublished - Sep 1 2012


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

ASJC Scopus subject areas

  • Medicine(all)


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