amg-458 and Glioma

amg-458 has been researched along with Glioma* in 1 studies

Other Studies

1 other study(ies) available for amg-458 and Glioma

Article	Year
Selective MET Kinase Inhibition in MET-Dependent Glioma Models Alters Gene Expression and Induces Tumor Plasticity. Molecular cancer research : MCR, 2017, Volume: 15, Issue:11 The receptor tyrosine kinase (RTK) MET represents a promising tumor target in a subset of glioblastomas. Most RTK inhibitors available in the clinic today, including those inhibiting MET, affect multiple targets simultaneously. Previously, it was demonstrated that treatment with cabozantinib (MET/VEGFR2/RET inhibitor) prolonged survival of mice carrying orthotopic patient-derived xenografts (PDX) of the MET-addicted glioblastoma model E98, yet did not prevent development of recurrent and cabozantinib-resistant tumors. To exclude VEGFR2 inhibition-inflicted blood-brain barrier normalization and diminished tumor distribution of the drug, we have now investigated the effects of the novel MET-selective inhibitor Compound A in the orthotopic E98 xenograft model. Topics: Aminopyridines; Animals; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Glioma; HT29 Cells; Humans; Mice; Protein Kinase Inhibitors; Pyrazoles; Sequence Analysis, RNA; Small Molecule Libraries; Xenograft Model Antitumor Assays	2017

Article

Year

Selective MET Kinase Inhibition in MET-Dependent Glioma Models Alters Gene Expression and Induces Tumor Plasticity.

Molecular cancer research : MCR, 2017, Volume: 15, Issue:11

The receptor tyrosine kinase (RTK) MET represents a promising tumor target in a subset of glioblastomas. Most RTK inhibitors available in the clinic today, including those inhibiting MET, affect multiple targets simultaneously. Previously, it was demonstrated that treatment with cabozantinib (MET/VEGFR2/RET inhibitor) prolonged survival of mice carrying orthotopic patient-derived xenografts (PDX) of the MET-addicted glioblastoma model E98, yet did not prevent development of recurrent and cabozantinib-resistant tumors. To exclude VEGFR2 inhibition-inflicted blood-brain barrier normalization and diminished tumor distribution of the drug, we have now investigated the effects of the novel MET-selective inhibitor Compound A in the orthotopic E98 xenograft model.

Topics: Aminopyridines; Animals; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Glioma; HT29 Cells; Humans; Mice; Protein Kinase Inhibitors; Pyrazoles; Sequence Analysis, RNA; Small Molecule Libraries; Xenograft Model Antitumor Assays

2017