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Upregulation of Flt3 is a passive event in Hoxa9/Meis1-induced acute myeloid leukemia in mice

A Staffas1,2, L S Arabanian1, S Y Wei1,3

  • 1Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.

Oncogene
|September 13, 2016
PubMed

Insights

The study found that Flt3 (FMS-like tyrosine kinase 3) is not required for acute myeloid leukemia (AML) progression driven by HOXA9 and MEIS1. High Flt3 expression on leukemia cells acts as a marker, not a driver, in this AML subtype.

Area of Science:

  • Molecular Biology
  • Hematology
  • Cancer Research

Background:

  • HOXA9, MEIS1, and FLT3 are frequently upregulated in acute myeloid leukemia (AML).
  • Hoxa9 and Meis1 cooperate to induce aggressive AML with high Flt3 expression in mice.
  • The precise role of Flt3 in Hoxa9/Meis1-induced leukemogenesis requires further definition.

Purpose of the Study:

  • To elucidate the role of Flt3 in AML characterized by high HOXA9 and MEIS1 expression.
  • To investigate the impact of Flt3 inhibition and Flt3-ligand deficiency on leukemogenesis.

Main Methods:

  • Treatment of Hoxa9/Meis1-induced AML mouse models with the Flt3 inhibitor AC220.
  • Utilizing a Flt3-ligand (FL-/-) knockout mouse model.
  • Assessing leukemogenesis upon co-overexpression of Flt3 and Hoxa9.

Main Results:

  • Flt3 inhibition did not impede AML development in mice overexpressing Hoxa9 and Meis1.
  • Hoxa9/Meis1 cells induced AML in FL-/- mice as rapidly as in wild-type mice, with reduced organ infiltration in FL-/- mice.
  • Leukemic cells expressed high Flt3 levels irrespective of Flt3-ligand presence, indicating Flt3 is a passive marker.

Conclusions:

  • The upregulation of Flt3 associated with HOXA9 and MEIS1 is not essential for leukemic progression.
  • Flt3 plays a limited role in the invasiveness of Hoxa9/Meis1-induced AML.
  • Flt3 functions primarily as a marker rather than a driver in this specific AML context.

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