| Project/Area Number |
22591430
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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 |
General surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAGINO Masato 名古屋大学, 大学院・医学系研究科, 教授 (20237564)
YOKOYAMA Yukihiro 名古屋大学, 医学部附属病院, 講師 (80378091)
KOKURYO Toshio 名古屋大学, 大学院・医学系研究科, 特任講師 (60378023)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 微小転移 / 微小転移関連遺伝子 / FAK / 微小転移開連遺伝子 |
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| Research Abstract |
FAK (focal adhesion kinase), a metastasis related gene, was highly expressed in the EpCAM-positive breast cancer cells. FAK siRNA suppressed the invasion and the motility in breast cancer cell lines. Subsequently, we focused on Girdin (Girders of actin filament), which was actin-binding protein and a substrate of AKT. Immunohistochemistry revealed that the expression of Girdin was significantly associated with lymph node metastasis. We next examined the combined expression of Ki67 and Girdin in the 73 luminal type breast cancer cases. 5-year disease free survivals in Ki67-positive and Girdin-positive cases were the worst, in comparison with other cases. Our data suggested that Girdin canbe a marker for the lymph node metastasis and poor prognosis in patients with breast cancer.
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