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• W2006945705 abstract "Abstract To verify molecular mechanisms by which leukemia stem cells (LSCs) maintain a dormant state, we explored the activity of the major prosurvival signal pathways in CD34 + /CD38 − compartment, supposed to contain LSCs, and CD34 + /CD38 + counterparts from patients with acute myelogenous leukemia (AML, n = 11) by fluorescence‐activated cell sorting (FACS). CD34 + /CD38 − cells expressed a greater amount of p‐janus kinase 2 (JAK2) and p‐signal transducer and activator of transcription 5 (STAT5) than CD34 + /CD38 + counterparts in all patients except for one case. In addition, we found that CD34 + /CD38 − cells were relatively resistant to cytarabine‐ and the inhibitor of the fms‐like tyrosine kinase 3 (FLT3)‐mediated growth inhibition, as measured by the clonogenic assay. Interestingly, blockade of JAK2/STAT5 signaling by the specific JAK2 inhibitor AZ960 stimulated cell cycling in CD34 + /CD38 − cells in conjunction with downregulation of cyclin‐dependent kinase inhibitor p21 waf1 and sensitized these cells to the growth inhibition mediated by cytarabine and the FLT3 kinase inhibitor. Moreover, exposure of CD34 + /CD38 − cells to AZ960 potently induced apoptosis in parallel with downregulation of antiapoptotic protein Bcl‐xL, as measured by Western blot analysis. Taken together, JAK2/STAT5 signaling may be a promising molecular target to eradicate CD34 + /CD38 − leukemia cells in individuals with AML." @default.
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• W2006945705 date "2011-02-26" @default.
• W2006945705 modified "2023-10-17" @default.
• W2006945705 title "Inhibition of signal transducer and activator of transcription 5 by the inhibitor of janus kinases stimulates dormant human leukemia CD34⁺/CD38⁻ cells and sensitizes them to antileukemia agents" @default.
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• W2006945705 doi "https://doi.org/10.1002/ijc.25806" @default.
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