| Project/Area Number |
26830068
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
Isagawa Takayuki 東京医科歯科大学, 難治疾患研究所, 助教 (40418637)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
Takeda Norihiko 東京大学, 医学部循環器内科, 特任講師 (40422307)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 腫瘍間質 / マクロファージ / WNT / NFkB / 癌間質 / 炎症 |
|---|
| Outline of Final Research Achievements |
It is well known that tumor stroma is composed of inflammatory, vascular and fibroblastic cells and has a pivotal role in cancer development and progression. In this study, we analyzed a xenograft model of pancreatic carcinoma using the tumor-stroma interactome, a method for analyzing cell interactions in the tumor tissue (which is composed of various cells), and identified WNT signal pathway as a novel signal pathway acting from the tumor to the stroma. Furthermore, we revealed that activation of the WNT signal pathway suppressed the inflammatory response of macrophages through the suppression of the NFkB pathway. These results suggest the possibility that the immune-regulatory mechanism mediated by WNT signaling of tumor cells induces immunological tolerance in tumor tissue.
|
