| Project/Area Number |
15K21113
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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 |
Tumor biology
Human genetics
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| Research Institution | Kyoto University |
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Principal Investigator |
Tanaka Azusa 京都大学, 医学研究科, 特別研究員(PD) (70749796)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | エピゲノム / 細胞分化 / 成人T細胞白血病 / クロマチン |
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| Outline of Final Research Achievements |
It is now accepted that the initiation and progression of cancer, traditionally seen as a genetic disease, also involves epigenetic aberrations. Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus and the etiological agent of adult T-cell leukemia-lymphoma (ATL). Here, we performed ATAC-seq on ATL cell samples and discovered global alterations in the chromatin status. For this experiment, we modified original ATAC-seq protocol to apply this method to limited number of cells in clinical samples. To characterize differences in chromatin accessibility in ATL cells and normal human CD4+ memory T cells, we searched for regions of gained and lost genome accessibility. Motif analysis of increased accessible sites in ATL cells identified a strong enrichment in bZIP family transcription factors. Now we are performing a knock down experiment to confirm the importance of this transcription factor.
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