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Perturbing LSD1 and WNT rewires transcription to synergistically induce AML differentiation.

Amir Hosseini1, Abhinav Dhall2, Nemo Ikonen3

  • 1Ludwig Institute for Cancer Research, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

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|April 16, 2025
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Summary
This summary is machine-generated.

This study shows that combining LSD1 inhibition and GSK3 inhibition effectively treats acute myeloid leukaemia (AML) by promoting cell differentiation and improving survival in mice.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Impaired cellular differentiation is a key characteristic of myeloid malignancies.
  • Differentiation therapy, using agents like ATRA and ATO, is effective in acute promyelocytic leukaemia but its broader applicability in AML is unclear.

Purpose of the Study:

  • To investigate the therapeutic potential of combining LSD1 inhibition (LSD1i) and GSK3 kinase inhibition (GSK3i) for acute myeloid leukaemia (AML).
  • To elucidate the underlying molecular mechanisms driving differentiation in AML cells treated with this combination therapy.

Main Methods:

  • Treatment of established AML cell lines and primary human AML cells with simultaneous LSD1i and GSK3i.
  • Evaluation of therapeutic differentiation, tumor burden, and survival in a patient-derived xenograft mouse model.
  • Mechanistic studies involving gene expression analysis, transcription factor induction (IRF7, β-catenin), and pathway analysis (Type I interferon, WNT pathway).

Main Results:

  • The combination of LSD1i and GSK3i robustly promoted therapeutic differentiation in AML cells.
  • This combination reduced tumor burden and significantly extended survival in a preclinical AML mouse model.
  • Mechanistically, the treatment activated the Type I interferon pathway and suppressed pro-oncogenic WNT signaling and cell cycle genes.

Conclusions:

  • Simultaneous inhibition of LSD1 and GSK3 represents a promising therapeutic strategy for AML.
  • The combination therapy rewires transcriptional programs to suppress stemness and promote differentiation, with potential implications for other WNT-driven cancers.