The role of Interleukin-6 family cytokines in repair and tumorigenesis in the lung.
| Project/Area Number |
20890116
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| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
KIDA Hiroshi Osaka University, 医学部附属病院, 特任助教(常勤) (80512988)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Mitsuhiro 大阪大学, 大学院・医学系研究科, 助教 (90359844)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,302,000 (Direct Cost: ¥2,540,000、Indirect Cost: ¥762,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,742,000 (Direct Cost: ¥1,340,000、Indirect Cost: ¥402,000)
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| Keywords | 幹細胞 / 肺癌 / Stat3 / ウレタン / ナフタレン / ノックアウトマウス / 気道上皮幹細胞 / 肺腫瘍 / 気道上皮修復 / インターロイキン-6 / gp130 / STAT3 / 肺特異的ノックアウトマウス |
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| Research Abstract |
Urethane-induced tumorigenesis was suppressed in the lungs of airway epithelium-specific knockout mice of Stat3 (Stat3^<Δ/Δ>) compared to control mice, suggesting that Stat3 in airway epithelium was required for the tumor growth in the lung. Immunohistochemistry did not show any significant differences in differentiation, proliferation or angiogenesis in the tumor. However, bronchoalveolar lavage (BAL) revealed that the local inflammation was significantly increased in the lung of Stat3^<Δ/Δ> compared to control mice, suggesting the possibility that tumor suppression was mediated by the increased inflammation in the lung of Stat3^<Δ/Δ>.
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Report
(3 results)
Research Products
(5 results)
