Overexpression of HGF/MET axis along with p53 inhibition induces de novo glioma formation in mice.

Yuan Qin,Anna Musket,Jianqun Kou,Johanna Preiszner,Barbara R Tschida,Anna Qin,Craig A Land,Ben Staal,Liang Kang,Kirk Tanner,Yong Jiang,John B Schweitzer,David A Largaespada,Qian Xie

Neuro-oncology advances（2020）

引用 8|浏览50

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摘要

Overexpression of the HGF/MET axis along with p53 attenuation may transform neural stem cells into GSCs, resulting in GBM formation in mice. These tumors are primarily driven by the MET RTK pathway activation and are sensitive to MET TKIs. The SB-hHgf.Met.ShP53 spontaneous mouse glioma model provides a useful tool for studying GBM tumor biology and MET-targeting therapeutics.

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关键词

HGF/MET signaling,genetically engineered mouse model,glioblastoma,glioma initiating cells,targeted therapy

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