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MET exon 14 deletion (METex14): finally, a frequent-enough actionable oncogenic driver mutation in non-small cell lung cancer to lead MET inhibitors out of “40 years of wilderness” and into a clear path of regulatory approval

   
@article{TLCR5983,
	author = {Thanyanan Reungwetwattana and Sai-Hong Ignatius Ou},
	title = {MET exon 14 deletion (METex14): finally, a frequent-enough actionable oncogenic driver mutation in non-small cell lung cancer to lead MET inhibitors out of “40 years of wilderness” and into a clear path of regulatory approval},
	journal = {Translational Lung Cancer Research},
	volume = {4},
	number = {6},
	year = {2015},
	keywords = {},
	abstract = {The hepatocyte growth factor (HGF) ligand and its receptor MET (mesenchymal-epithelial transition) tyrosine kinase receptor axis has long been demonstrated to be important in oncogenesis and metastasis in multiple tumor types. Mechanisms of dysregulation of the HGF-MET axis includes over-expression of the HGF ligand, activating point mutations in MET, MET gene amplification, MET protein over-expression and potentially MET rearrangements. Many structural different MET tyrosine kinase inhibitors (TKIs) have been developed to target the HGF-MET axis pathway but so far the results have been disappointing (1).},
	issn = {2226-4477},	url = {https://tlcr.amegroups.org/article/view/5983}
}