Development of mouse brain tumor models by epigenetic disturbance of imprinting genes
Project/Area Number |
15K15528
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Neurosurgery
|
Research Institution | Kochi University |
Principal Investigator |
FUKUDA Maki 高知大学, 医学部, 研究員 (20735691)
|
Co-Investigator(Kenkyū-buntansha) |
上羽 哲也 高知大学, 教育研究部医療学系臨床医学部門, 教授 (00314203)
八幡 俊男 高知大学, 教育研究部医療学系臨床医学部門, 助教 (40380323)
|
Project Period (FY) |
2015-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 脳腫瘍 / エピジェネティクス |
Outline of Final Research Achievements |
Tumor-specific metabolism influences epigenetic regulation in malignant brain tumor. Of these targeted molecules, TET1 and TET2 genes are involved in hydroxylation of methylated DNA and lead to DNA demethylation. In this study, the expression of TET1 and TET2 genes was examined in glioblastoma cells and tissues. There was no difference of expression of TET1 between cell lines, tumor, and normal tissue cells. On the other hand, TET2 was strongly expressed in tumor tissues, but not in normal tissue cells and cell lines. TET2 might play a role for glioblastomagenesis as well as TET1.
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Report
(3 results)
Research Products
(6 results)