Abstract
MET is a receptor tyrosine kinase being involved in a plethora of physiologic and developmental processes. MET-inhibitors, e.g. crizotinib, capmatinib or lenvatinib, are effective in cancers with MET exon 14 skipping mutations or with top-level MET amplifications. Emerging evidence indicates that also MET fusions represent a predictive biomarker for potentially effective MET inhibition. However, data on frequencies and subtypes of MET fusions among solid tumors are limited so far.
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