| Project/Area Number |
17H06803
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2017-08-25 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 膵癌 / Hes1 |
|---|
| Outline of Final Research Achievements |
During tumorigenesis, Hes1 starts to be expressed from precancerous lesions to pancreatic ductal adenocaricinomal (PDAC), howerever, the role of Hes1 in pancreatic tumorigenesis was not fully elucidated. In the present study, we demonstrated that Hes1 gene deletion dramatically suppressed the formation of pancreatic lesions in mice. We provide evidence that Hes1 plays essential roles in multiple steps of PDAC initiation by regulating Sox9 expression. The antitumor effect of a novel Hes1 inhibitor on pancreatic cancer cells in vitro and in vivo suggests that Hes1 could be a new preventive or therapeutic target for PDAC.
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| Academic Significance and Societal Importance of the Research Achievements |
膵癌は本邦における悪性腫瘍死亡原因の第5位を占め、未だに5年生存率が10%に満たない最難治癌であり、予後改善・新規治療薬の開発には、その病態解明が必須である。切除不能膵癌の化学療法の選択肢は未だに少なく、化学療法を行っても生存中央日数は1年に満たない。Hes1がその選択肢の一つになることができれば、膵癌の予後改善の寄与することが可能と考える。
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