| Project/Area Number |
24790347
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | Chiba University (2013)
The University of Tokyo (2012) |
|---|
Principal Investigator |
MATSUSAKA Keisuke 千葉大学, 医学(系)研究科(研究院), 助教 (40610150)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | エピジェネティクス / ウイルス学 / 病理学 / Epstein-Barr virus / DNAメチル化 |
|---|
| Research Abstract |
Gastric cancers (GCs) have a characteristic subgroup with Epstein-Barr virus (EBV) latent infection. EBV-positive (EBV(+)) GC showed extremely higher methylation phenotype and EBV infection induced genome-wide de novo DNA methylation in a low-methylation cell line, MKN7, resulting in acquisition of EBV(+) particular phenotype. In this study, we tried to clarify the mechanism to induce de novo DNA methylation through time-series analysis of DNA methylation focusing on both host cell and virus. As a result, the EBV genome methylation preceded to the host cellular genome methylation, which implied that there should be well-ordered mechanism through close interaction between EBV and host cells. Host cellular genome-wide methylation completed in only 4 weeks. This study might lead to breakthrough about the mechanism of induction of aberrant DNA methylation.
|
