High‐sensitive clinical diagnostic method for PTPRZ1‐MET and the characteristic protein structure contributing to ligand‐independent MET activation,CNS Neuroscience & Therapeutics

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High‐sensitive clinical diagnostic method for PTPRZ1‐MET and the characteristic protein structure contributing to ligand‐independent MET activation
CNS Neuroscience & Therapeutics ( IF 4.8 ) Pub Date : 2021-02-28 , DOI: 10.1111/cns.13627
Ruoyu Huang _{1,

2,

3,

4,

5} , Yanwei Liu _{1,

2,

3,

4,

5} , Kuanyu Wang _{1,

2,

3,

4,

5} , Zheng Wang _{1,

2,

3,

4,

5} , Chuanbao Zhang _{1,

2,

3,

4,

5} , Wei Zhang _{1,

2,

3,

4,

5} , Zheng Zhao _{1,

2,

3,

4,

5} , Guanzhang Li _{1,

2,

3,

4,

5} , Lijie Huang _{1,

2,

3,

4,

5} , Yuanhao Chang _{1,

2,

3,

4,

5} , Fan Zeng _{1,

2,

3,

4,

5} , Tao Jiang _{1,

2,

3,

4,

5} , Huimin Hu _{1,

2,

3,

4,

5}

Affiliation

PTPRZ1‐MET (ZM) is a critical genetic alteration driving the progression of lower‐grade glioma. Glioma patients harboring ZM could benefit from MET inhibitors. According to the remarkable role of ZM as a driver of glioma progression and indicator of MET inhibitor sensitivity, it is necessary to detect this alteration even when it presents in glioma with relatively fewer copies.

中文翻译：

PTPRZ1-MET 的高灵敏度临床诊断方法和有助于配体非依赖性 MET 激活的特征性蛋白质结构

PTPRZ1 - MET ( ZM ) 是推动低级别胶质瘤进展的关键基因改变。携带ZM的神经胶质瘤患者可以从 MET 抑制剂中受益。根据ZM作为神经胶质瘤进展的驱动因素和 MET 抑制剂敏感性指标的显着作用，即使它存在于具有相对较少拷贝的神经胶质瘤中，也有必要检测这种改变。

更新日期：2021-04-08

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