| Project/Area Number |
24592018
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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 | Tohoku University |
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Principal Investigator |
MOTOI Fuyuhiko 東北大学, 医学(系)研究科(研究院), 准教授 (30343057)
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| Co-Investigator(Kenkyū-buntansha) |
OHTSUKA Hideo 東北大学, 大学病院, 助教 (50451563)
TACHIKAWA Masanori 東北大学, 薬学系研究科, 准教授 (00401810)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 膵癌 / 化学療法 / 抗癌剤耐性 / 質量分析 / 抗癌剤 / 膵臓外科学 |
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| Outline of Final Research Achievements |
Most of pancreatic cancer is unresectable at the time of diagnosis. The recurrence rate is extremely high even after curative resection. We performed expression analysis of factors influencing the sensitivity for anti-cancer agents from the resected specimen and linked the clinical outcome to explore the potential mechanism of anti-cancer drug resistance. The natural resistance of pancreatic cancer cell lines was demonstrated by the observation of more than 1,000 times higher relative IC50 values of 5FU in vitro. The IC50 of most molecular-targetting agents against pancreatic cancer cells was higher than those of 5FU, suggesting poor clinical outcome of molecular-targetting agents. Only the protein expression level of deoxycytidine kinase (dCK) of resected cancer specimen, treated with gemcitabine (GEM) postoperatively, was significantly correlated with progression free survival of the patient, suggesting that dCK was an important factor for GEM resistance of pancreatic cancers.
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