| Project/Area Number |
22590857
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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 |
Respiratory organ internal medicine
|
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| Research Institution | Fujita Health University (2011-2012)
Nagoya University (2010) |
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Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
SATO Mitsuo 名古屋大学, 医学系研究科, 講師 (70467281)
橋本 直純 名古屋大学, 医学部附属病院, 助教 (30378020)
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| Project Period (FY) |
2010 – 2012
|
| 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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 呼吸器病学 / 肺がん / リンパ節 / EMT / HIF1α / VEGF / 内科 / 呼吸器内科 / 肺癌 / リンパ節転移 |
|---|
| Research Abstract |
Based on our recognition for the importance of tumor microenvironment(TM), TM induces acquisition of malignant phenotype such as epithelial-mesenchymal transition (EMT), resulting in metastasis into lymph nodes. In this study, persistent tissue hypoxia might be involved in tumor tissue in an in vivo orthotopic intrapulmonary implantation model. Persistent hypoxia also induced the stabilized HIF1α expression in lung cancer cells. Transduction of HIF1α into lung cancers with the Doxycycline inducible gene expression system caused de novo VEGF-A expression. Taken together with the evidence of increasing VEGF receptor expression lymphatic endothelial cells in sentinel lymph nodes, hypoxia as TM in lung cancers might be a therapeutic target for the metastasis into lymph nodes and lymphangiogenesis.
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