2014 Fiscal Year Final Research Report
The role of TLR4 signaling pathway and exosome heat shock protein in chronic myeloid leukemia
Project/Area Number |
23590309
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
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Research Institution | Tokyo Women's Medical University |
Principal Investigator |
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Project Period (FY) |
2011-04-28 – 2015-03-31
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Keywords | 慢性骨髄性白血病 / 熱ショックタンパク質 / Toll様受容体 / 薬剤耐性 |
Outline of Final Research Achievements |
Although BCR-ABL tyrosine-kinase inhibitor (imatinib) is effective front-line therapy for chronic myeloid leukemia (CML), drug resistance is a well-recognized problem. In the present study, we found that the stimulation of TLR4 signaling pathway up-regulates BCR-ABL protein levels and may contribute to imatinib resistance. Heat shock proteins appear to be involved in the protein stability of BCR-ABL. Our findings provide new insight into the role of the TLR4 signaling pathway in drug resistance, and may have implications for the development of new therapeutic strategies to overcome drug resistance in CML.
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Free Research Field |
分子薬理学
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