Association of stemness preservation with oncogenesis of odontogenic epithelium within the intraosseous microenvironment
Project/Area Number |
15K11066
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
|
Research Institution | Tohoku University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
清水 良央 東北大学, 歯学研究科, 助教 (30302152)
及川 麻理子 東北大学, 歯学研究科, 助教 (00712902)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 歯原性腫瘍 / 腫瘍発生 / 骨内進展 |
Outline of Final Research Achievements |
Regulator molecules associated with hypoxic condition, cell development, proliferation, and differentiation were examined to clarify the effect of stemness preservation in oncogenesis of odontogenic epithelium under the intraosseous microenvironment. Hypoxia-related molecules, HIF-1 and CA IX, were greater in ameloblastoma than in tooth germ, and solid ameloblastoma showed high reactivity as compared with unicystic ameloblastoma. Measurement of CD34-positive microvessels were correlated positively with HIF-1 and CA IX. Cell proliferation signaling pathways , MAPK, Akt, and STAT3, were activated in ameloblastoma rather than tooth germ, and BRAF mutations were detected only in ameloblastoma but not in tooth germ. Translocation of cell development-related gene EWSR1 was confirmed in clear cell odontogenic carcinoma but not in other celar cell tumors by FISH method.
|
Report
(4 results)
Research Products
(34 results)
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
[Book] 頭頸部腫瘍II2015
Author(s)
熊本裕行(森永正二郎 高田隆 長尾俊孝編)
Total Pages
301
Publisher
文光堂
Related Report