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Low c-Kit expression identifies primitive, therapy-resistant CML stem cells.

Mansi Shah1, Harish Kumar1, Shaowei Qiu1,2

  • 1Division of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, Alabama, USA.

JCI Insight
|November 22, 2022
PubMed
Summary
This summary is machine-generated.

Primitive, drug-resistant leukemia stem cells in chronic myeloid leukemia (CML) persist after treatment. Targeting low c-Kit expressing CML long-term hematopoietic stem cells (LT-HSCs) may eliminate residual disease.

Keywords:
Adult stem cellsGrowth factorsHematologyLeukemiasOncology

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Area of Science:

  • Hematology
  • Cancer Biology
  • Stem Cell Biology

Background:

  • Tyrosine kinase inhibitors (TKIs) are effective against chronic myeloid leukemia (CML), but residual leukemia stem cells cause relapse.
  • Long-term hematopoietic stem cells (LT-HSCs) are heterogeneous, with primitive, drug-resistant subpopulations poorly understood.

Purpose of the Study:

  • To characterize drug-resistant CML LT-HSC subpopulations.
  • To investigate the role of c-Kit expression and stem cell factor (SCF) in CML stem cell persistence and drug resistance.

Main Methods:

  • Utilized a transgenic CML mouse model.
  • Analyzed LT-HSC subpopulations based on c-Kit expression.
  • Investigated the effects of stem cell factor (SCF) and its deletion on normal and CML LT-HSCs.
  • Assessed cell cycling, quiescence, and gene expression signatures.
  • Examined human CML LT-HSCs post-TKI treatment.

Main Results:

  • Long-term engraftment and leukemogenic capacity in CML were restricted to c-KITlo LT-HSCs.
  • SCF exposure enhanced differentiation of CML LT-HSCs, while SCF deletion increased CML LT-HSCs and decreased normal LT-HSCs.
  • CML c-KITlo LT-HSCs exhibited reduced cell cycling, enhanced quiescence, and inflammatory gene expression.
  • SCF treatment depleted CML progenitors but not LT-HSCs post-TKI; human CML LT-HSCs with low/absent c-KIT were enriched after TKI treatment.

Conclusions:

  • CML LT-HSCs with low c-Kit expression represent primitive, quiescent, drug-resistant leukemia-initiating cells.
  • These c-KITlo CML LT-HSCs are a critical target for eradicating persistent CML.
  • Understanding LT-HSC heterogeneity is crucial for developing curative therapies for CML.