| Project/Area Number |
24590924
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Nagoya City University |
|---|
Principal Investigator |
okamoto yasuyuki 名古屋市立大学, 医学(系)研究科(研究院), 研究員 (60444973)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
hayashi katsuki 名古屋市立大学, 医学研究科, 助教 (00405200)
澤田 武 金沢大学, その他の研究科, 准教授 (60345626)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
sawada takeshi 金沢大学, 医薬保健学総合研究科, 准教授 (60345626)
|
|---|
| Project Period (FY) |
2012-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | GIST / DNA methylation / DNAメチル化 |
|---|
| Outline of Final Research Achievements |
Regarding SDH deficient GIST, the promoter of the markers (PAX3, REC8 and P16) are markedly methylated. So these markers should be used for either KIT mutated GIST or PDGFR mutated GIST. From pathway analysis using illumina 450K array data, we found abnormally methylated genes among SDH deficient GIST were enriched in PI3K/Akt signaling pathway, which are downstream of the KIT receptor. It suggests that abnormal DNA methylations induced by SDH deficient cause development of GIST with neither KIT mutations nor PDGFR mutations. Gene set analysis based on genome wide DNA methylation and transcriptome profiling revealed the relationship between G protein-coupled receptors (GPCRs) and malignant GIST.
|
