2013 Fiscal Year Final Research Report
Pulmonary dysfunction as adverse effect is attributed to the inhibition of the novel gefitinib target GAK.
| Project/Area Number |
24700978
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Osaka University |
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Principal Investigator |
NAITO Yoko 大阪大学, 免疫学フロンティア研究センター, 特任研究員 (10553026)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | ゲフィチニブ / 腫瘍抑制 / 間質性肺炎 / GAK |
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| Research Abstract |
The aim of this study is to reveal the mechanism by which gefitinib (iressa), an inhibitor of epithelial growth factor receptor (EGFR), suppress tumor progression and cause pulmonary alveolar dysfunction as adverse effect. We found that gefitinib inhibited GAK kinase activity and inhibition of GAK activity caused dysregulation of EGF-EGFR signaling by aberrant controlling of phosphorylation and endocytosis. We clarified that GAK expression was increased in several cancer and inhibition of GAK suppressed cancer progression by inducing apoptosis. These results may be useful for development of a gefitinib-drived drug which prevent side effect associated with gefitinib therapy and have a more beneficial effect on tumor suppression.
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