| Project/Area Number |
20591572
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
MIYANARI Nobutomo Kumamoto University, 医学部附属病院, 非常勤診療講師 (90336230)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Naoko 熊本大学, 医学部附属病院, 非常勤診療医師 (20452899)
BABA Hideo 熊本大学, 大学院・生命科学研究部, 教授 (20240905)
YOSHIDA Naoya 熊本大学, 医学部附属病院, 非常勤診療医師 (60467983)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 食道外科学 / mTOR / RAD001 / ラミミン-332 / 食道癌 / 消化器癌 |
|---|
| Research Abstract |
Inactivation of the AKT pathway by laminin-332 blocking antibody suppressed the invasiveness of esophageal cancer cell line. The addition of the purified laminin-332 activated the AKT pathway and increased the invasiveness of cell line. These results indicate that Laminin-332 could contribute to the malignant behavior of esophageal cancer through AKT pathway. mTOR is a key molecule in the AKT pathway and is increasingly important as a potential target for anticancer therapy. Thus, we focused on revealing clinical usefulness of mTOR inhibitor in esophageal cancer. p-mTOR overexpression was independently associated with poor prognosis in ESCC, supporting the potential for mTOR as a therapeutic target for ESCC. We are currently performing further in vitro and in vivo study to clarify the antitumor effect of RAD001 (mTOR inhibitor) on ESCC.
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