c-MET as a potential therapeutic target and biomarker in cancer.
c-MET as a potential therapeutic target and biomarker in cancer.
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DOI：
10.1177/1758834011422557
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发表时间：
2011-11-01
影响因子：
4.9
通讯作者：
Tsao, Ming-Sound
中科院分区：
文献类型：
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作者：
Sierra, J Rafael;Tsao, Ming-Sound
受体酪氨酸激酶c-MET及其配体肝细胞生长因子（HGF）调节刺激细胞增殖、侵袭和血管生成的多种细胞过程。本综述概述了支持c-MET或HGF/c-MET信号通路作为基于非小细胞肺癌（NSCLC）、胃癌、卵巢癌、胰腺癌、甲状腺癌、乳腺癌、头颈癌、结肠癌和肾癌中c-MET和/或HGF高频率过表达、活化、扩增的个性化癌症治疗相关靶点的证据。此外，还讨论了小分子抑制剂（tivantinib [ARQ 197]）、c-MET/HGF抗体（rilotumumab和MetMAb）和c-MET靶向治疗耐药机制的当前知识。
The receptor tyrosine kinase c-MET and its ligand, hepatocyte growth factor (HGF), regulate multiple cellular processes that stimulate cell proliferation, invasion and angiogenesis. This review provides an overview of the evidence to support c-MET or the HGF/c-MET signaling pathway as relevant targets for personalized cancer treatment based on high frequencies of c-MET and/or HGF overexpression, activation, amplification in non-small cell lung carcinoma (NSCLC), gastric, ovarian, pancreatic, thyroid, breast, head and neck, colon and kidney carcinomas. Additionally, the current knowledge of small molecule inhibitors (tivantinib [ARQ 197]), c-MET/HGF antibodies (rilotumumab and MetMAb) and mechanisms of resistance to c-MET-targeted therapies are discussed.