@article{oai:repo.qst.go.jp:00046094,
 author = {Hasegawa, Yuzo and Iwadate, Yasuo and Saito, Shigeyoshi and Aoki, Ichio and Saeki, Naokatsu and Yonemitsu, Yoshikazu and et.al and 長谷川 祐三 and 岩立 康男 and 齋藤 茂芳 and 青木 伊知男},
 issue = {10},
 journal = {Molecular Therapy},
 month = {Jul},
 note = {Glioblastoma multiforme (GM), the most frequent primary malignant brain tumor, is highly invasive due to the expression of proteases, including urokinase-type plasminogen activator (uPA). Here, we show the potential of our new and powerful recombinant Sendai virus (rSeV) showing uPA-specific cell-to-cell fusion activity [rSeV/dMFct14 (uPA2), named "BioKnife"] for GM treatment, an effect that was synergistically enhanced by arming BioKnife with the interferon-beta (IFN-beta) gene. BioKnife killed human GM cell lines efficiently in a uPA-dependent fashion, and this killing was prevented by PA inhibitor-1. Rat gliosarcoma 9L cells expressing both uPA and its functional receptor uPAR (9L-L/R) exhibited high uPA activity on the cellular surface and were highly susceptible to BioKnife. Although parent 9L cells (9L-P) were resistant to BioKnife and to BioKnife expressing IFN-beta (BioKnife-IFNbeta), cell-cell fusion of 9L-L/R strongly facilitated the expression of IFN-beta, and in turn, IFN-beta significantly accelerated the fusion activity of BioKnife. A similar synergy was seen in a rat orthotopic brain GM model with 9L-L/R in vivo; therefore, these results suggest that BioKnife-IFNbeta may have significant potential to improve the survival of GM patients in a clinical setting.},
 pages = {1778--1786},
 title = {Urokinase-targeted fusion by oncolytic Sendai virus eradicates orthotopic glioblastomas by pronounced synergy with interferon-beta gene},
 volume = {18},
 year = {2010}
}