Analysis of MET kinase domain rearrangement in NSCLC

MET, a hepatocyte growth factor receptor, is expressed throughout epithelial and endothelial cells. Functional characterization shows that activation of c-Met orchestrates signaling pathways culminating in cell cycle regulations, facilitating activities such as cell proliferation, invasion, survival, angiogenesis, and motility. MET amplification and MET exon 14 skipping have been observed in various cancers, and was demonstrated to be not only an actionable mutation to crizotinib, but also one of the resistance mechanisms to EGFR tyrosine kinase inhibitors [1,2].

Source: Lung Cancer - May 14, 2020 Category: Cancer & Oncology Authors: Minglei Zhuo, Zhen Liang, Yuting Yi, Nan Wu, Xue Yang, Jia Zhong, Xiaohan Chen, Yi Huang, Zicheng Yu, Chang Liu, Xiaoling Zeng, Wenguang Gu, Jun Zhao Source Type: research