BCR-ABL1-induced leukemogenesis and autophagic targeting by arsenic trioxide

Dennis J. Goussetis, Elias Gounaris, Leonidas C. Platanias*

*Corresponding author for this work

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

We have recently shown that arsenic trioxide (As2O3) is a potent inducer of autophagic degradation of the BCR-ABL1 oncoprotein, which is the cause of chronic myeloid leukemia (CML) and Ph+ acute lymphoid leukemia (Ph+ ALL). Our recently published work has shown that pharmacological inhibition of autophagy or molecularly targeting of elements of the autophagic machinery partially reverses the suppressive effects of As2O3 on primitive leukemic precursors from CML patients. Altogether, our studies have provided direct evidence that arsenic-induced, autophagy-mediated, degradation of BCR-ABL1 is an important mechanism for the generation of the effects of As2O3 on BCR-ABL1 transformed leukemic progenitors. These studies raise the potential of future clinical-translational efforts employing combinations of arsenic trioxide with autophagy-modulating agents to promote elimination of early leukemic progenitors and, possibly, leukemia-initiating stem cells.

Original languageEnglish (US)
Pages (from-to)93-94
Number of pages2
JournalAutophagy
Volume9
Issue number1
DOIs
Publication statusPublished - Jan 2013

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Keywords

  • Arsenic trioxide
  • Autophagy
  • BCR-ABL1
  • Cell death
  • Leukemia

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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