Rapid Radiographic and Clinical Improvement After Treatment of a MET-Amplified Recurrent Glioblastoma With a Mesenchymal-Epithelial Transition Inhibitor

作者：Andrew S. Chi, Tracy T. Batchelor, Eunice Lee Kwak, Jeffrey William Clark, Daphne L. Wang, Keith D. Wilner, David N. Louis, Anthony John Iafrate · 发表于：Journal of Clinical Oncology · 年份：2011 · DOI：10.1200/jco.2011.38.4586 · 被引用次数：107 · 研究领域：Glioma Diagnosis and Treatment、Cancer Cells and Metastasis、Cancer Genomics and Diagnostics

A 62-year-old right-handed white woman presented with periodic motion-related nausea and vertigo.On physical examination, she had only mild high-frequency hearing loss on the right side.Cranial magnetic resonance imaging (MRI) revealed an unresectable contrast-enhancing lesion measuring 3.6 cm in maximal horizontal diameter within the genu of the corpus callosum, with surrounding abnormal T2/fluid-attenuated inversion recovery (FLAIR) hyperintensity.Stereotactic biopsy of the contrast-enhancing lesion established the diagnosis of glioblastoma (GBM), WHO grade 4.Her tumor tissue was tested for genetic abnormalities using a comprehensive panel that included screening for commonly mutated loci in 15 cancer-related genes using a multiplex polymerase chain reaction platform (SNaPshot, Version 3; Applied Biosystems, Carlsbad, CA) 1 ; amplification of the mesenchymal-epithelial transition (MET), epidermal growth factor receptor (EGFR), and plateletderived growth factor receptor A (PDGFRA) genes using fluorescence in situ hybridization (FISH); status of chromosomes 1p and 19q by FISH; and O-6-methylguanine-DNA methyltransferase (MGMT) promoter DNA methylation status by methylationspecific polymerase chain reaction.Her tumor was found to have MET gene amplification by a dual-color FISH assay using probes for the MET locus (Fig 1, pink dots) and centromere 7 (Fig 1, aqua dots), which served as a copy-number control.In addition, the MGMT promoter was methylated.