| Project/Area Number |
26462070
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Yokohama City University |
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Principal Investigator |
ENDO Itaru 横浜市立大学, 医学研究科, 教授 (60211091)
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| Co-Investigator(Kenkyū-buntansha) |
廣島 幸彦 横浜市立大学, 医学研究科, 客員研究員 (60718021)
森 隆太郎 横浜市立大学, 医学部, 講師 (90596412)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 膵癌 / 浸潤 / 転移 / 免疫 / 膵炎 / Kras / CRMP4 / マウスモデル / リン酸化 / CDK5 / GSK3β |
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| Outline of Final Research Achievements |
Pancreatic cancer has been an aggressive malignancy. Recently, stroma in tumor is reported to be associated with cancer-cell proliferation, apoptosis, differentiation, and invasion in several cancers. Previously, we examined proteins expressing in the stroma of pancreatic tumors or of normal pancreas, and found that CRMP4 differentially expressed in pancreatic tumor stroma compared to normal pancreatic tissue. Of all the CRMPs, only CRMP4 was differentially expressed in pancreatic cancer tissues. CRMP4 staining was highly correlated with poor differentiation and liver metastasis. In this project, we revealed that caerulein-induced pancreatitis augments the expression of CRMP4 in vivo experiment. Sequencially, we investigated the role of CRMP4 in pancreatic cancer precursor lesions in gene engineered mouse model. Our results suggested that CRMP4 is significantly associated with initiation and progression of pancreatic cancer.
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