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ID 53014
フルテキストURL
著者
Ishida, Joji Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Onishi, Manabu Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Kurozumi, Kazuhiko Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Ichikawa, Tomotsugu Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Fujii, Kentaro Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Shimazu, Yosuke Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Oka, Tetsuo Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
Date, Isao Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
抄録
Glioblastoma is known to secrete high levels of vascular endothelial growth factor (VEGF), and clinical studies with bevacizumab, a monoclonal antibody to VEGF, have demonstrated convincing therapeutic benefits in glioblastoma patients. However, its induction of invasive proliferation has also been reported. We examined the effects of treatment with cilengitide, an integrin inhibitor, on bevacizumab-induced invasive changes in glioma. U87 Delta EGFR cells were stereotactically injected into the brain of nude mice or rats. Five days after tumor implantation, cilengitide and bevacizumab were administered intraperitoneally three times a week. At 18 days after tumor implantation, the brains were removed and observed histopathologically. Next, the bevacizumab and cilengitide combination group was compared to the bevacizumab monotherapy group using microarray analysis. Bevacizumab treatment led to increased cell invasion in spite of decreased angiogenesis. When the rats were treated with a combination of bevacizumab and cilengitide, the depth of tumor invasion was significantly less than with only bevacizumab. Pathway analysis demonstrated the inhibition of invasion-associated genes such as the integrin-mediated cell adhesion pathway in the combination group. This study showed that the combination of bevacizumab with cilengitide exerted its anti-invasive effect. The elucidation of this mechanism might contribute to the treatment of bevacizumab-refractory glioma.
発行日
2014-04
出版物タイトル
Translational Oncology
7巻
2号
出版者
Elsevier Science Inc
開始ページ
292
終了ページ
302
ISSN
1944-7124
資料タイプ
学術雑誌論文
関連URL
http://ousar.lib.okayama-u.ac.jp/metadata/52970
言語
English
OAI-PMH Set
岡山大学
論文のバージョン
publisher
査読
有り
DOI
Web of Sience KeyUT