| Project/Area Number |
26670625
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
SUZUKI Motoshi 名古屋大学, 医学(系)研究科(研究院), 講師 (80236017)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUI Takayuki 名古屋大学, 医学部附属病院, 病院講師 (70463198)
WAKAHARA Keiko 名古屋大学, 医学部附属病院, 病院講師 (00631433)
KATO Sei-ichi 名古屋大学, 大学院医学系研究科, 講師 (30584669)
Nishida Atsushi 千葉大学, 大学院薬学研究院, 教授 (80130029)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 肺がん / がん幹細胞 / 低分子化合物 / 肺癌 / 抗癌剤 / 分子標的治療薬 |
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| Outline of Final Research Achievements |
We collected clinical lung cancer specimens and transplanted each of in the immune-deficient mice. Xenografts were recovered after tumor formation, collagenase-treated, and sorted for CD166 positive population. In a cell line, the CD166 positive cells successfully formed secondary tumors in mice. We performed database analysis to figure out a gene candidate which may contribute to the cancer initiating cell nature. By using the above cell line, we established a stable cell line that is associated with a knockdown of this gene, and inoculated thousands of cells in mice. Results are forthcoming. We also screened for an inhibitor against this gene product. Among the 2000 candidates, we found a compound that inhibits the activity. To decrease the EC50 value, we started optimization of this compound.
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