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Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up
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A mechanism for increased sensitivity of acute myeloid leukemia to mitotoxic drugs

Svetlana B Panina1, Natalia Baran2, Fabio H Brasil da Costa1,3

  • 1Department of BioSciences, Rice University, Houston, TX, USA.

Cell Death & Disease
|August 15, 2019
PubMed

Insights

Mitochondria-targeting drugs (mitocans) show increased effectiveness against acute myeloid leukemia (AML) due to specific metabolic defects. Combining mitocans with glycolytic inhibitors offers a potent and selective anti-leukemia therapy.

Area of Science:

  • Oncology
  • Mitochondrial Biology
  • Cancer Metabolism

Background:

  • Mitochondria are crucial in cancer development.
  • The varying susceptibility of cancers to mitocans and their mechanisms remain poorly understood.
  • Cancer type influences response to mitochondrial-targeting drugs.

Purpose of the Study:

  • To investigate why certain cancers are more sensitive to mitocans.
  • To identify the mechanisms behind mitocan efficacy in different tumor types.
  • To evaluate the therapeutic potential of mitocans, alone and in combination, for acute myeloid leukemia (AML).

Main Methods:

  • Comparative analysis of tumor response to mitocan treatment across various cancer types.
  • Assessment of mitochondrial metabolic function in AML cells.
  • Evaluation of synergistic effects of combined mitocan (CCCP) and glycolytic inhibitor (2-deoxyglucose) treatment in AML cells, including primary patient samples.

Main Results:

  • Cancer type is a significant predictor of mitocan treatment response.
  • Acute myeloid leukemia (AML) exhibits heightened sensitivity to mitocans.
  • AML cells possess distinct mitochondrial metabolic defects contributing to their sensitivity.
  • Combined mitocan and glycolytic inhibitor treatment shows significant synergy in AML cells.
  • Therapeutic doses are well-tolerated by normal blood cells, unlike cancer cells.

Conclusions:

  • Mitochondrial defects in AML cells underpin their sensitivity to mitocans.
  • Combination therapy with mitocans and glycolytic inhibitors demonstrates potent anti-leukemia effects.
  • Mitochondria represent a promising and selective therapeutic target for AML treatment.

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