Drug development of MET inhibitors: targeting oncogene addiction and expedience

被引：692

作者：

Comoglio, Paolo M. ^{[1
]}

Giordano, Silvia ^{[1
]}

Trusolino, Livio ^{[1
]}

机构：

[1] Univ Turin, Sch Med, Inst Canc Res & Treatment IRCC, Div Mol Oncol, I-10060 Turin, Italy

来源：

NATURE REVIEWS DRUG DISCOVERY | 2008年 / 7卷 / 06期

关键词：

D O I：

10.1038/nrd2530

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The MET tyrosine kinase stimulates cell scattering, invasion, protection from apoptosis and angiogenesis, thereby acting as a powerful expedient for cancer dissemination. MET can also be genetically selected for the long-term maintenance of the primary transformed phenotype, and some tumours appear to be dependent on (or 'addicted' to) sustained MET activity for their growth and survival. Because of its dual role as an adjuvant, pro-metastatic gene for some tumour types and as a necessary oncogene for others, MET is a versatile candidate for targeted therapeutic intervention. Here we discuss recent progress in the development of molecules that inhibit MET function and consider their application in a subset of human tumours that are potentially responsive to MET-targeted therapies.

引用

页码：504 / 516

页数：13

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