Article
Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors.
Cancer discovery - 1 Aug 2015
Frampton Garrett M, Ali Siraj M, Rosenzweig Mark, Chmielecki Juliann, Lu Xinyuan, Bauer Todd M, Akimov Mikhail, Bufill Jose A, Lee Carrie, Jentz David, Hoover Rick, Ou Sai-Hong Ignatius, Salgia Ravi, Brennan Tim, Chalmers Zachary R, Jaeger Savina, Huang Alan, Elvin Julia A, Erlich Rachel, Fichtenholtz Alex, Gowen Kyle A, Greenbowe Joel, Johnson Adrienne, Khaira Depinder, McMahon Caitlin, Sanford Eric M, Roels Steven, White Jared, Greshock Joel, Schlegel Robert, Lipson Doron, Yelensky Roman, Morosini Deborah, Ross Jeffrey S, Collisson Eric, Peters Malte, Stephens Philip J, Miller Vincent A
Abstract excerpt
UNLABELLED: Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility to targeted MET inhibitors. Recurrent somatic splice site alterations at MET exon 14 (METex14) that result in exon skipping and MET activation have been characterized, but their full diversity and prevalence across tumor types are unknown. Here, we report analysis of...
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