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Chemosensitizing AML cells by targeting bone marrow endothelial cells.

Raphael C Bosse1, Briana Wasserstrom1, Amy Meacham1

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Targeting blood vessels with combretastatins disrupts acute myeloid leukemia (AML) protection by bone marrow endothelial cells (BMECs). This combination therapy enhances AML cell death and promotes complete tumor regression in mice.

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Area of Science:

  • Hematology
  • Oncology
  • Vascular Biology

Background:

  • Refractory acute myeloid leukemia (AML) presents a significant therapeutic challenge.
  • Blood vessels within the bone marrow microenvironment may act as protective sanctuaries for AML cells.
  • Bone marrow endothelial cells (BMECs) play a role in maintaining AML cell quiescence.

Purpose of the Study:

  • To investigate the role of BMECs in protecting AML cells.
  • To evaluate the efficacy of targeting BMECs with combretastatins in combination with chemotherapy.
  • To explore a novel therapeutic strategy for refractory AML.

Main Methods:

  • Co-culture of AML cells with BMECs.
  • Treatment of co-cultures with tubulin-binding combretastatins.
  • Assessment of BMEC phenotype, adhesion molecule expression, and AML cell cycle status.
  • In vivo studies using mice xenograft models.

Main Results:

  • Combretastatins altered BMEC morphology and reduced adhesion molecule expression (VCAM-1, VE-cadherin).
  • Combretastatins treatment dislodged AML cells from BMECs and promoted cell cycle progression.
  • Combination therapy with combretastatins and cytotoxic chemotherapy resulted in enhanced AML cell death.
  • Complete AML regression was observed in mice treated with the combination therapy.

Conclusions:

  • BMECs contribute to AML resistance by providing a protective niche.
  • Vascular-targeting agents like combretastatins can disrupt this protective niche.
  • Combination therapy of combretastatins and chemotherapy offers a promising strategy for treating refractory AML.