Targeting Leukemia Stem Cells with Novel Therapeutic Agents
- Authors: Yaoyu Chen1, Cong Peng2, Dongguang Li3, Shaoguang Li4
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View Affiliations Hide Affiliations1 Division of Hematology/Oncology, Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA 2 Current address: Department of Hematology/Oncology, Children’s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA 3 School of Computer and Security Science, Edith Cowan University, 2 Bradford Street, Mount Lawley, WA 6050, Australia 4 Division of Hematology/Oncology, Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
- Source: Advances in Anticancer Agents in Medicinal Chemistry: Volume 2 , pp 397-409
- Publication Date: June 2013
- Language: English
Chronic myeloid leukemia (CML) is induced by the BCR-ABL oncogene, a product of Philadelphia (Ph) chromosome. The BCR-ABL kinase inhibitor imatinib is a standard treatment for Ph+ leukemia, and has been shown to induce a complete hematologic and cytogenetic response in most chronic phrase CML patients. However, imatinib does not cure CML, and one of the reasons is that imatinib does not kill leukemia stem cells (LSCs) in CML both in vitro and in vivo. Recently, several new targets or drugs have been reported to inhibit LSCs in cultured human CD34+ CML cells or in mouse model of BCR-ABL induced CML, including an Alox5 pathway inhibitor, Hsp90 inhibitors, omacetaxine, hedgehog inhibitor and BMS-214662. Specific targeting of LSCs but not normal stem cell is a correct strategy for developing new anti-cancer therapies in the future.
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