Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by a chromosome translocation that generates the BCR-ABL oncogene encoding a constitutively activated tyrosine kinase. Although BCR-ABL tyrosine kinase inhibitors (TKIs) are highly effective in treating CML at chronic phase, a number of patients develop drug resistance due to the inability of TKIs to kill leukemia stem cells (LSCs). Similar to other types of hematopoietic malignancies, LSCs in CML are believed to be a rare cell population responsible for leukemia initiation, disease progression, and drug resistance. Therefore, a full understanding of the biology of LSCs will help to develop novel therapeutic strategies for effective treatment of CML to possibly reach a cure. In recent years, a significant progress has been made in studying the biology of LSCs in both animal models and human patients at cellular and molecular levels, providing a basis for designing and testing potential molecular targets for eradicating LSCs in CML.
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