The epigenetics of leukemic cell drug resistance
Project/Area Number |
24791052
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Pediatrics
|
Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
|
Keywords | 癌 / 遺伝子 / 発現制御 |
Outline of Final Research Achievements |
We confirmed that the demethylating agent (decitabine) enhances the cytotoxic effect of anti-leukemic agents such as clofarabine and etoposide synergistically, and the cytotoxic effect is depend on caspase-3/7 activity. Then, we confirmed that decitabine increase mRNA expression levels of BID, BAX, BAD, PUMA, CASP3. Although, decitabine did not demethylate the CpG of BID, BAX, BAD, CASP3. Therefore, we carried out genome-wide gene expression studies and epigenome-wide association studies. The results showed that decitabine demethylate the CpG of AATK and increase its mRNA expression.
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Report
(4 results)
Research Products
(5 results)