作者: Neelesh Sharma , Alex A. Adjei
关键词: Foretinib 、 Receptor tyrosine kinase 、 Gene mutation 、 Cancer research 、 Clinical trial 、 C-Met 、 Medicine 、 Paracrine signalling 、 Autocrine signalling 、 Bioinformatics 、 Cabozantinib
摘要: The c-MET (mesenchymal-epithelial transition factor) pathway is dysregulated in many human cancers and promotes tumor growth, invasion dissemination. receptor tyrosine kinase can be activated via gene mutation, amplification, protein overexpression and/or a ligand-dependent autocrine/paracrine loop. Abnormalities signaling have been reported to correlate with poor clinical outcomes drug resistance patients cancer. Significant progress has made advancement of inhibitors through trials. A robust pipeline high-quality targeting different aspects activation currently being explored phase I, II III trials across multiple types. Preliminary data demonstrate promising activity these agents, along an acceptable toxicity profile. In this manuscript, the pharmacological profile drugs available from ongoing are discussed.