C-MET as a new therapeutic target for the development of novel anticancer drugs

被引：53

作者：

Canadas, Israel ^{[4
]}

Rojo, Federico ^{[3
,4
]}

Arumi-Uria, Montserrat ^{[2
,4
]}

Rovira, Ana ^{[4
]}

Albanell, Joan

Arriola, Edurne ^{[1
,4
]}

机构：

[1] Hosp del Mar, Dept Oncol, ES-08003 Barcelona, Spain

[2] Hosp del Mar, Dept Pathol, ES-08003 Barcelona, Spain

[3] Capio Fdn Jimenez Diaz, Dept Pathol, Madrid, Spain

[4] Hosp del Mar, Mol Therapeut & Biomarkers Canc Lab, IMIM, ES-08003 Barcelona, Spain

来源：

CLINICAL & TRANSLATIONAL ONCOLOGY | 2010年 / 12卷 / 04期

关键词：

MET; HGF; Small molecule inhibitors; Antibodies; HEPATOCYTE GROWTH-FACTOR; RECEPTOR TYROSINE KINASE; CELL LUNG-CANCER; SMALL-MOLECULE INHIBITOR; FACTOR SCATTER FACTOR; SOMATIC MUTATIONS; IN-VIVO; MET/HGF RECEPTOR; GENE AMPLIFICATION; INVASIVE PHENOTYPE;

D O I：

10.1007/s12094-010-0501-0

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

MET is a tyrosine kinase receptor that, upon binding of its natural ligand, the hepatocyte growth factor (HGF), is phosphorylated and subsequently activates different signalling pathways involved in proliferation, motility, migration and invasion. MET has been found to be aberrantly activated in human cancer via mutation, amplification or protein overexpression. MET expression and activation have been associated with prognosis in a number of tumour types and predict response to MET inhibitors in preclinical models. Here we review the HGF/MET signalling pathway, its role in human cancer and the different inhibitory strategies that have been developed for therapeutic use.

引用

页码：253 / 260

页数：8

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