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

Megan A. Hatlen, Lan Wang, Stephen D Nimer

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

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
Pages (from-to)248-262
Number of pages15
JournalFrontiers of Medicine in China
Volume6
Issue number3
DOIs
StatePublished - Sep 1 2012
Externally publishedYes

Fingerprint

Acute Myeloid Leukemia
Leukemia
Therapeutics
Protein Transport
Transcription Factors
Pediatrics
Genes
Proteins

Keywords

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

ASJC Scopus subject areas

  • Medicine(all)

Cite this

AML1-ETO driven acute leukemia : Insights into pathogenesis and potential therapeutic approaches. / Hatlen, Megan A.; Wang, Lan; Nimer, Stephen D.

In: Frontiers of Medicine in China, Vol. 6, No. 3, 01.09.2012, p. 248-262.

Research output: Contribution to journalArticle

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