Molecular signatures of chronic myeloid leukemia stem cells

被引：43

作者：

Chen Y. ^{[1
]}

Li S. ^{[2
,3
]}

机构：

[1] Department of Oncology, Novartis Institutes for Biomedical Research, Cambridge, MA 02139

[2] Department of Medicine, Division of Hematology/Oncology, University of Massachusetts Medical School, Worcester, MA 01605

[3] Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605

来源：

Biomarker Research | / 1卷 / 1期

关键词：

BCR-ABL; Biomarker; Cancer stem cells; CML; Hematopoietic stem cells; Leukemic stem cells;

D O I：

10.1186/2050-7771-1-21

中图分类号：

学科分类号：

摘要：

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. © 2013 Chen and Li; licensee BioMed Central Ltd.

引用

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