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Chronic myelogenous leukemia (CML)

BCR-ABL tyrosine kinase; macrophage inflammatory protein-1a (CCL3; MIP1A)

Mouse studies suggest inhibiting CCL3 signaling could help treat CML. In a newly developed, nonirradiated mouse model of CML using BCR-ABL-expressing, leukemia-initiating cells, Ccl3 knockout delayed disease relapse following cessation of Gleevec imatinib therapy and increased survival compared with no knockout. Next steps include studies to identify progenitor cell subsets that compete with leukemia-initiating cells and to understand how such cells are maintained in the bone marrow niche.
Novartis AG markets Gleevec to treat CML and gastrointestinal stromal tumors.

SciBX 6(46); doi:10.1038/scibx.2013.1316
Published online Dec. 5, 2013

Patent application filed; licensing details available from Kanazawa University

Baba, T. et al. J. Exp. Med.; published online Oct. 28, 2013;
Contact: Tomohisa Baba, Kanazawa University, Ishikawa, Japan