Rowth factorscatter factor. Nature. 1995;373(6516):70205. 11. Maina F, Hilton MC, Ponzetto C, Davies
Rowth factorscatter factor. Nature. 1995;373(6516):70205. 11. Maina F, Hilton MC, Ponzetto C, Davies AM, Klein R. Met receptor signaling is needed for sensory nerve development and HGF promotes axonal development and survival of sensory neurons. Genes Dev. 1997;11(24):3341350. 12. Bladt F, Riethmacher D, Isenmann S, Aguzzi A, Birchmeier C. Essential part for the c-met receptor within the migration of myogenic precursor cells into the limb bud. Nature. 1995;376(6543):76871. 13. Chmielowiec J, Borowiak M, Morkel M, et al. c-Met is essential for wound healing within the skin. J Cell Biol. 2007;177(1):15162. 14. Huh CG, Aspect VM, S chez A, Uchida K, Conner EA, Thorgeirsson SS. Hepatocyte growth factorc-met signaling pathway is necessary for effective liver regeneration and repair. Proc Natl Acad Sci U S A. 2004;101(13):4477482. 15. Liu Y. Hepatocyte growth aspect in kidney fibrosis: therapeutic potential and mechanisms of action. Am J Physiol Renal Physiol. 2004;287(1):F7 16. 16. Schmidt L, Duh FM, Chen F, et al. Germline and CDK11 Species somatic mutations inside the tyrosine kinase domain from the MET proto-oncogene in papillary renal carcinomas. Nat Genet. 1997;16(1):683. 17. Graveel CR, London CA, Vande Woude GF. A mouse model of activating Met mutations. Cell Cycle. 2005;four(four):51820. 18. Nakajima M, Sawada H, Yamada Y, et al. The prognostic significance of amplification and overexpression of c-met and c-erb B-2 in human gastric carcinomas. Cancer. 1999;85(9):1894902. 19. Kuniyasu H, Yasui W, Kitadai Y, Yokozaki H, Ito H, Tahara E. Frequent amplification from the c-met gene in scirrhous form stomach cancer. Biochem Biophys Res Commun. 1992;189(1):22732. 20. Fischer U, M ler HW, Sattler HP, Feiden K, Zang KD, Meese E. Amplification from the MET gene in glioma. Genes Chromosomes Cancer. 1995;12(1):635. 21. Samuelson E, Levan K, Adamovic T, Levan G, Horvath G. ALK5 MedChemExpress Recurrent gene amplifications in human form I endometrial adenocarcinoma detected by fluorescence in situ hybridization. Cancer Genet Cytogenet. 2008;181(1):250. 22. Beau-Faller M, Ruppert AM, Voegeli AC, et al. MET gene copy number in non-small cell lung cancer: molecular evaluation in a targeted tyrosine kinase inhibitor na e cohort. J Thorac Oncol. 2008;3(4):33139. 23. Zeng ZS, Weiser MR, Kuntz E, et al. c-Met gene amplification is related with advanced stage colorectal cancer and liver metastases. Cancer Lett. 2008;265(two):25869. 24. Scagliotti GV Novello S, von Pawel J. The emerging role of MET , HGF inhibitors in oncology. Cancer Treat Rev. 2013;39(7):79301. 25. Dulak AM, Gubish CT, Stabile LP, Henry C, Siegfried JM. HGFindependent potentiation of EGFR action by c-Met. Oncogene. 2011; 30(33):3625635. 26. Engelman JA, Zejnullahu K, Mitsudomi T, et al. MET amplification results in gefitinib resistance in lung cancer by activating ERBB3 signaling. Science. 2007;316(5827):1039043. OncoTargets and Therapy 2014:Conclusion and future directionsThe ubiquity of MET-pathway activation in cancer plus the malignant phenotype that it confers on METmutated, -amplified, or -overexpressed tumors make sure that this is an attractive therapeutic target for many cancers. Pharmacological inhibition of this pathway has clear positive aspects with regards to response and survival, albeit in restricted numbers to date. It is clear that to optimize these benefits clinical trials has to be enriched for sufferers with demonstrable MET-pathway dysregulation; what is significantly less clear is the most effective signifies by which to achieve this. Robust standardization and validation of as.