| Project/Area Number |
25462107
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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 | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAJIMA HIDEHIRO 金沢大学, 大学病院, 講師 (00436825)
太田 哲生 金沢大学, 医学系, 教授 (40194170)
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| Co-Investigator(Renkei-kenkyūsha) |
OHTA TETSUO 金沢大学, 医学系, 教授 (40194170)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | EMT / 血小板凝集抑制 / HDAC阻害薬 / タキサン系抗がん剤 / タキサン系抗癌剤 / 膵頭部癌 / 放射線治療 / 膵星細胞 |
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| Outline of Final Research Achievements |
We evaluated the effect of valproic acid (VPA) and taxan for radiosensitivity in esophageal cancer, and investigated inhibitory effect of Epithelial-mesenchymal transition (EMT) using VPA and taxan for pancreatic stellate. Correlation EMT and platelet aggregation in the microenvironment of pancreatic cancer was clarified. VPA enhances cancer cells radiosensitivity by chromatin decondensation and down regulation of DNA double strand break repair proteins. Docetaxel (DTX) induced G1 and G2-M accumulation in esophageal cancer cell, respectively. Low dose DTX could yield radiosensitivity with induction of G1 arrest, although low dose DTX had limited cytotoxic effect. It has been shown that taxan (paclitaxel) and histone deacetylase (HDAC) inhibitor (sodium valproate) suppress the induction of EMT in pancreatic stem cell line in current study. But it has also been shown that the suppression of platelet aggregation has an important role of inhibition of the EMT in pancreatic cancer.
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