Department of Medicine, Division of Hematology/Oncology
BCR-ABL tyrosine kinase inhibitors (TKIs) are effective in controlling Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) are unlikely to cure the disease because TKIs are unable to eradicate leukemia stem cells (LSCs) responsible for the disease relapse even after tyrosine kinase inhibition. In addition, the TKI resistance of LSCs is not associated with the BCR-ABL kinase domain mutations. These observations indicate that TKI-insensitive LSCs and TKI-sensitive leukemic progenitor cells are biologically different, which leads us to believe that LSCs and more differentiated leukemic cells have different genetic mechanisms. Further study of LSCs to identify the novel gene signatures and mechanisms that control the function and molecular phenotype of LSCs is critical. In this mini-review, we will discuss our current understanding of the biology of LSCs and novel genes that could serve as a molecular signature of LSCs in CML. These novel genes could also serve as potential targets for eradicating LSCs in CML.
BCR-ABL, Leukemic stem cells, CML, Biomarker, Hematopoietic stem cells, Cancer stem cells
Rights and Permissions
Copyright 2013 Chen and Li; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
DOI of Published Version
Chen Y, Li S. Molecular signatures of chronic myeloid leukemia stem cells. Biomark Res. 2013 Jun 6;1(1):21. doi: 10.1186/2050-7771-1-21. Link to article on publisher's site
Chen Y, Li S. (2013). Molecular signatures of chronic myeloid leukemia stem cells. University of Massachusetts Medical School Faculty Publications. https://doi.org/10.1186/2050-7771-1-21. Retrieved from https://escholarship.umassmed.edu/faculty_pubs/310