Carrie R. Graveel

TL;DR: It is concluded that high MET expression in human breast cancers significantly correlated with estrogen receptor negative/ERBB2 negative tumors and with basal breast cancers and may be a rational therapeutic target.

TL;DR: Results demonstrate that activating Met mutations and met amplification play key roles in promoting tumorigenesis in vivo and show that different mutations in the Met kinase domain can influence the types of cancers that develop.

TL;DR: Comprehensive systems biology analysis of metabolic perturbations, combined siRNA and tyrosine kinase inhibitor screens identified a core set of TCA cycle and fatty acid pathways whose perturbation sensitizes TNBC cells to small molecule targeting of receptor tyrosin kinases.

TL;DR: The unique features ofMET and hepatocyte growth factor/scatter factor (HGF/SF) structure and signaling, mutational activation, genetic mouse models of MET and HGF/ SF, and MET-targeted therapeutics are examined.

TL;DR: Glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to type I MET inhibitors, as well as a mixed response to a METex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed.