MET receptor in oncology: From biomarker to therapeutic target

被引:17
|
作者
Malik, Raeva [1 ]
Mambetsariev, Isa [2 ]
Fricke, Jeremy [2 ]
Chawla, Neal [3 ]
Nam, Arin [2 ]
Pharaon, Rebecca [2 ]
Salgia, Ravi [2 ]
机构
[1] George Washington Univ Hosp, Washington, DC USA
[2] City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA
[3] Advocate Illinois Masonic Med Ctr, Dept Med, Chicago, IL USA
来源
RECEPTOR TYROSINE KINASES | 2020年 / 147卷
关键词
HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; GENE COPY NUMBER; NF-KAPPA-B; TYROSINE KINASE RECEPTOR; C-MET; SCATTER FACTOR; ACQUIRED-RESISTANCE; SOMATIC MUTATIONS; MITOCHONDRIAL FISSION;
D O I
10.1016/bs.acr.2020.04.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
First discovered in the 1984, the MET receptor tyrosine kinase (RTK) and its ligand hepatocyte growth factor or HGF (also known as scatter factor or SF) are implicated as key players in tumor cell migration, proliferation, and invasion in a variety of cancers. This pathway also plays a key role during embryogenesis in the development of muscular and nervous structures. High expression of the MET receptor has been shown to correlate with poor prognosis and resistance to therapy. MET exon 14 splicing variants, initially identified by us in lung cancer, is actionable through various tyrosine kinase inhibitors (TKIs). For this reason, this pathway is of interest as a therapeutic target. In this chapter we will be discussing the history of MET, the genetics of this RTK, and give some background on the receptor biology. Furthermore, we will discuss directed therapeutics, mechanisms of resistance, and the future of MET as a therapeutic target.
引用
收藏
页码:259 / 301
页数:43
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