| Project/Area Number |
21790788
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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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 | Showa University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 肺癌 / 肺障害 / 上皮成長因子受容体 / 腫瘍壊死因子 / 急性肺障害 / EGFR / TNF-alpha / apoptosis / TACE / アポトーシス / 肺線維症 |
|---|
| Research Abstract |
EGFR tyrosine kinase activity protects TNF-induced lung epithelial cells apoptosis and this might be the mechanism of EGFR tyrosine kinase inhibitor (TKI)-induced lung injury. In this study, to the purpose of clarifying the mechanisms, we employed the SPC/TNF-transgenic mice, which over-expressed TNF in alveolar type 2 cells under the control of the human surfactant protein C promoter, resulted in interstitial pneumonia and pulmonary fibrosis chronically. EGFR-TKI, Gefitinib was orally administrated for this mice, then we observed worsened the lung injury. This novel observation has significant implications for understanding the role of EGFR in maintaining human lung epithelial cell homeostasis in an environment of inflammation, injury/repair, such as inflammation-associated carcinogenesis and cancer promotion.
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