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A FOXO1-induced oncogenic network defines the AML1-ETO preleukemic program.

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  • 1Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.

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Targeting FOXO1, a key driver of self-renewal in preleukemia stem cells, can prevent acute myeloid leukemia (AML) relapse. Blocking FOXO1 inhibits proliferation in both preleukemic and leukemic cells, offering a new therapeutic strategy.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Acute myeloid leukemia (AML) relapse is often driven by preleukemia stem cells.
  • The t(8;21) translocation is associated with a specific subtype of AML.
  • FOXO1 is typically a tumor suppressor but is upregulated in t(8;21) AML.

Purpose of the Study:

  • To investigate the role of FOXO1 in the self-renewal of preleukemic stem cells in t(8;21) AML.
  • To determine if FOXO1 could be a therapeutic target for preventing AML relapse.

Main Methods:

  • Studied the effect of FOXO1 expression in human CD34+ cells.
  • Utilized genome-wide binding studies to analyze FOXO1 and AML1-ETO (AE) binding sites.
  • Assessed the impact of genetic and pharmacological FOXO1 ablation on cancer cell proliferation and clonogenicity.

Main Results:

  • Increased FOXO1 drives aberrant self-renewal in AE-expressing preleukemic cells.
  • FOXO1 activates a stem cell signature in preleukemic and t(8;21) AML cells.
  • FOXO1 and AE share binding sites, with FOXO1 activating key self-renewal genes.
  • Inhibition of FOXO1 reduced the proliferation and clonogenicity of AE cells and AML cell lines.

Conclusions:

  • FOXO1 plays a critical role in the self-renewal of preleukemic stem cells in t(8;21) AML.
  • Targeting FOXO1 presents a promising therapeutic strategy for eliminating preleukemic and leukemic stem cells.
  • Blocking FOXO1 may prevent AML relapse by targeting the root cause of disease recurrence.