| Project/Area Number |
24591937
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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 | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KONNO Hiroyuki 浜松医科大学, 医学部, 教授 (00138033)
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| Co-Investigator(Renkei-kenkyūsha) |
KITAGAWA Masatoshi 浜松医科大学, 医学部, 教授 (50294971)
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 消化管間質腫瘍 / マイクロアレイ / 癌幹細胞 / 遺伝子発現 / SLIT2 / 分子標的薬 / 細胞周期 / 生物学的マーカー / 分子標的治療 |
|---|
| Outline of Final Research Achievements |
Gstrointestinal stromal tumors (GIST) can be treated with tyrosine kinase inhibitors (TKIs) such as imatinib, however; it is difficult to cure them with TKIs alone. In the present study, we have identified characteristics of cancer stem cell-like populations in GIST using cDNA macroarray analyses. In addition, we sought to address mechanisms underlying the clinically malignant phenotype of intestinal GIST and found that expression levels of SLIT2 protein were lower in intestinal GIST compared with gastric GIST. These results suggest that there remain important mechanisms underlying GIST malignant transformation that can be novel molecular markers as well as therapeutic targets of GIST.
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