2013 Fiscal Year Final Research Report
Role of survivin in EGFR inhibitor-induced apoptosis in non-small cell lung cancers positive for EGFR mutations.
| Project/Area Number |
23501316
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Clinical oncology
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| Research Institution | Kinki University |
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Principal Investigator |
OKAMOTO Kunio 近畿大学, 医学部附属病院, 助教 (90460865)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAGAWA Kazuhiko 近畿大学, 医学部, 教授 (40298964)
OKAMOTO Isamu 九州大学, 医学部, 准教授 (10411597)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 臨床腫瘍学 / 分子標的治療 |
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| Research Abstract |
The molecular mechanism by which epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) induce apoptosis in non-small cell-lung cancer (NSCLC) cells that are positive for activating mutations of the EGFR remains unclear. In this study, we report the effects of the EGFR-TKI gefitinib on expression of the antiapoptotic protein survivin that have functional consequences in EGFR mutation-positive NSCLC cells. Immunoblot analysis revealed that gefitinib downregulated survivin expression, likely through inhibition of the PI3K-AKT signaling pathway, in NSCLC cells positive for EGFR mutation. Stable overexpression of survivin attenuated gefitinib-induced apoptosis and also inhibited the antitumor effect of gefitinib in human tumor xenografts. Our results indicate that downregulation of survivin plays a pivotal role in gefitinib-induced apoptosis in EGFR mutation-positive NSCLC cells.
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[Journal Article] High-dose dexamethasone plus antihistamine prevents colorectal cancer patients treated with modified FOLFOX6 from hypersensitivity reactions induced by oxaliplatinHigh-dose dexamethasone plus antihistamine prevents colorectal cancer patients treated with modified FOLFOX6 from hypersensitivity reactions induced by oxaliplatin2011
Author(s)
Kidera Y, Satoh T, Ueda S, Okamoto W, Okamoto I, Fumita S, Yonesaka K, Hayashi H, Makimura C, Okamoto K, Kiyota H, Tsurutani J, Miyazaki M, Yoshinaga M, Fujiwara K, Yamazoe Y, Moriyama K, Tsubaki M, Chiba Y, Nishida S, Nakagawa K
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Journal Title
Int J Clin Oncol
Volume: 16(3)
Pages: 244-249
Peer Reviewed
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