Critical molecular pathways in cancer stem cells of chronic myeloid leukemia.

Abstract

Inhibition of BCR-ABL with kinase inhibitors in the treatment of Philadelphia-positive (Ph(+)) chronic myeloid leukemia (CML) is highly effective in controlling but not curing the disease. This is largely due to the inability of these kinase inhibitors to kill leukemia stem cells (LSCs) responsible for disease relapse. This stem cell resistance is not associated with the BCR-ABL kinase domain mutations resistant to kinase inhibitors. Development of curative therapies for CML requires the identification of crucial molecular pathways responsible for the survival and self-renewal of LSCs. In this review, we will discuss our current understanding of these crucial molecular pathways in LSCs and the available therapeutic strategies for targeting these stem cells in CML.

• Authors: Y Chen, C Peng, C Sullivan, D Li, S Li
• Journal: Leukemia (Leukemia) Vol. 24 Issue 9 Pg. 1545-54 (Sep 2010) ISSN: 1476-5551 [Electronic] England
• PMID: 20574455 (Publication Type: Journal Article, Review)

Chemical References

• Antineoplastic Agents
• Protein Kinase Inhibitors

Topics

• Animals
• Antineoplastic Agents (therapeutic use)
• Disease Models, Animal
• Genes, abl
• Humans
• Leukemia, Myelogenous, Chronic, BCR-ABL Positive (drug therapy, pathology)
• Mice
• Mice, Transgenic
• Mutation
• Neoplastic Stem Cells
• Protein Kinase Inhibitors (therapeutic use)