| Project/Area Number |
25870564
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
Biological pharmacy
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| Research Institution | Osaka University (2014)
University of Miyazaki (2013) |
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Principal Investigator |
KANEDA Kazuko 大阪大学, 医学(系)研究科(研究院), 特任助教(常勤) (00533209)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | インテグリン / 転写因子 / 薬剤耐性 / 白血病 / がん / 抗体医薬 / 接着分子 |
|---|
| Outline of Final Research Achievements |
EVI1 is one of the candidate oncogenes for human acute myeloid leukemia (AML).High EVI1 expression (EVI1high) is a risk factor for AML with poor outcome. We reported that expression of ITGA6 is associated with drug-resistance and increased cell adhesion, resulting in poor prognosis. We found that treating EVI1high leukemia cells with neutralizing antibodies against ITGA6/B4 resulted in an enhanced responsiveness to anti-cancer drugs and a reduction of their cell adhesion ability. The expression of ITGA6/B4 are significantly elevated in cells from relapsed and EVI1high AML cases and EVI1high AML cell lines; therefore, ITGA6/B4 might represent an important therapeutic target for both refractory and EVI1high AML. Neutralizing antibody against ITGA6/B4 might be expected as new drug combined administration with anti-cancer drug. We also clarified the regulation system of ITGA6/B4 via EVI1. This might be useful for development of new drug for EVI1high leukemia with bad prognosis.
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