Abnormal differentiation and instability of microRNA regulation in pancreatic carcinogenesis
Project/Area Number |
15K19046
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Human pathology
|
Research Institution | The University of Tokyo |
Principal Investigator |
Tanaka Mariko 東京大学, 大学院医学系研究科(医学部), 助教 (50645710)
|
Research Collaborator |
Fukayama Masashi
Ishikawa Shumpei
Katoh Hiroto
Isagawa Takayuki
Yamamoto Hiroyuki
Abe Jun
Yamagishi Makoto
Hasegawa Kiyoshi
Arita Junichi
Sakamoto Yoshihiro
Kokudo Takashi
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 膵がん / EVI1 / microRNA / 発がん / 膵発がん / KRAS / miRNA / 膵癌 |
Outline of Final Research Achievements |
I previously revealed the importance of claudin-18 and EVI1 in pancreatic carcinogenesis and identified the EVI1-miRNA96-KRAS axis. Based on our results, I tried to reveal the molecular mechanism to promote pancreatic carcinogensis with a central focus on EVI1 and microRNA. Consequently, I revealed that EVI1 promote pancreatic carcinogenesis by a new pathway, EVI1-miRNA96-Glypican1. I also built a basis for miRNA expression profile of pancreatic cancer cells and preneoplastic pancreatic cancer cells. These results are important to shed light on unsolved pancreatic carcinogensis.
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Report
(4 results)
Research Products
(4 results)