A novel recombinant immunotoxin-based therapy targeting wild-type and mutant EGFR improves survival in murine models of glioblastoma.

A novel recombinant immunotoxin-based therapy targeting wild-type and mutant EGFR improves survival in murine models of glioblastoma.
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DOI:
10.4161/onci.26852
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发表时间:
2013-12-01
期刊:
影响因子:
7.2
通讯作者:
Bigner DD
Bigner DD
中科院分区:
医学2区
文献类型:
--
作者:
Chandramohan V;Bigner DD

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编码野生型 (wt) 表皮生长因子受体 (EGFR) 的基因的扩增和 EGFR 缺失突变体(通常称为 EGFRvIII)的过度表达都是胶质母细胞瘤的标志。我们最近报道了一种新型重组免疫毒素 D2C7-(scdsFv)-PE38KDEL,它同时靶向 wt EGFR 和 EGFRvIII,对已建立的小鼠神经胶质瘤表现出有效的抗肿瘤作用。
Both the amplification of the gene coding for wild-type (wt) epidermal growth factor receptor (EGFR) and the overexpression of the EGFR deletion mutant, commonly known as EGFRvIII, are hallmarks of glioblastoma. We have recently reported a novel, recombinant immunotoxin, D2C7-(scdsFv)-PE38KDEL, that targets both wt EGFR and EGFRvIII, exhibiting potent antineoplastic effects against established murine gliomas.
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