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Area of Science:

  • Hematology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Acute myeloid leukemia (AML) initiation is driven by multiple mutations that reprogram progenitor cell identity.
  • FLT3 internal tandem duplication (FLT3ITD) mutations cooperate with various initiating mutations, occurring in both pediatric and adult AML.
  • The distinct genetic contexts of pediatric versus adult AML may lead to different FLT3ITD-induced transcriptional programs and therapeutic vulnerabilities.

Purpose of the Study:

  • To investigate whether FLT3ITD induces distinct transcriptional programs and therapeutic vulnerabilities when paired with pediatric versus adult AML-initiating mutations.
  • To compare AML evolution in mouse models carrying Flt3ITD/NUP98-HOXD13 (pediatric-biased) or Flt3ITD/Runx1DEL (adult-biased) mutation pairs.

Main Methods:

  • Single-cell analyses
  • Epigenome profiling
  • Comparative mouse modeling of AML evolution

Main Results:

  • Flt3ITD/NUP98-HOXD13 (pediatric) and Flt3ITD/Runx1DEL (adult) mutation pairs exhibited distinct interactions and transcriptional outcomes.
  • Flt3ITD/NHD13 drove the emergence of a pre-AML population, unlike the aberrant myeloid progenitor expansion seen with Flt3ITD/Runx1DEL.
  • Flt3ITD/NHD13 cooperatively targeted genes enriched in human NUP98-translocated AML and hijacked type I interferon signaling.
  • Blocking interferon signaling delayed AML initiation and extended survival in the Flt3ITD/NHD13 model.

Conclusions:

  • Common AML driver mutations like FLT3ITD can utilize different transformation mechanisms depending on the genetic context.
  • Pediatric-biased NUP98 fusions confer an actionable interferon dependence in AML.
  • Targeting interferon signaling represents a potential therapeutic strategy for a subset of AML patients with NUP98 fusions.