| Project/Area Number |
22591437
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
OZAKI Nobuyuki 熊本大学, 医学部附属病院, 非常勤診療医師 (40551255)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Hideo 熊本大学, 大学院・生命科学研究部, 教授 (20240905)
CHIKAMOTO Akira 熊本大学, 医学部附属病院, 講師 (10419640)
ISHIKO Takatoshi 熊本大学, 医学部附属病院, 准教授 (00343351)
TAKAMORI Hiroshi 熊本大学, 医学部附属病院, 非常勤診療医師 (90363514)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | PSTI / SPINK1 / TATI / 膵癌 / 慢性膵炎 / EGFR / 大腸癌 |
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| Research Abstract |
We aimed for the treatment strategy which assumed pancreatic cancer and elucidation ofa new receptor with PST. About a new receptor, we were not able to identify an effectivereceptor except EGFR. So, we established chronic pancreatitis model mouse of two kindsof onset mechanism by controlling PSTI gene expression using gene change technology andexamined activation of a pancreas stellate cell concerned with pancreatic fibrosis, Krasgene, EGFR family gene, expression of INK4a gene. We showed an abnormal increase withKi67 positive acini cell which formed duct -like structure. Expression of a Kras gene,an EGFR family gene was already present in conditions of chronic pancreatitis, and itwas suggested that it was a transition stage to precancerosis.
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