Drug development of MET inhibitors: targeting oncogene addiction and expedience

By P. Comoglio, S. Giordano, Livio Trusolino. Nature reviews. Drug discovery, 2008

845 citations recorded by the source corpus.

Subfields: Hepatology, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/284deff2b12f1dc7627abe685b2a6474f6f1f26d

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In Hepatology

In Molecular Biology

In Pathology and Forensic Medicine

Peter A. Jones

Citations in the corpus

MET signalling: principles and functions in development, organ regeneration and cancer (2010, background): “and it drives the malignant progression of several different types of tumour”
Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? (2009, background): “By exploiting the genetic differences between normal cells and cancer cells, several molecular-targeted drugs, such as imatinib (Gleevec; Novartis) and trastuzumab (Herceptin; Genentech/Roche), show promising therapeutic activity and few toxic side effect”
Pathogenesis, Diagnosis, and Management of Cholangiocarcinoma (2013, background): “In mice, overexpression of ERBB2 led to formation of tumors along the biliary epithelium.48 Hepatocyte growth factor (hepapoietin A; scatter factor) (HGF) is a stromal paracrine mediator that regulates tumor invasiveness and metastasis.49–51 Activation of MET, the receptor for HGF, up-regulates seve”
Epigenetic Modifications as Therapeutic Targets (2010, background): “A classic example of oncogene addiction is mesenchymal-epithelial transition factor (MET), a tyrosine kinase that acts as a receptor for hepatocyte growth factor and controls tissue homeostasis in normal cell”
Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer (2013, neutral): “The MET gene, encoding the tyrosine kinase receptor for Hepatocyte Growth Factor, has been shown to have an oncogenic role in several human tumors, where it becomes constitutively activated as a consequence of gene amplification, overexpression, activating mutations or autocrine stimulation (37).”
An overview of the c-MET signaling pathway (2011, background): “This cell surface receptor is expressed in epithelial cells of many organs, including the liver, pancreas, prostate, kidney, muscle and bone marrow, during both embryogenesis and adulthood [Comoglio et al. 2008].”
A census of amplified and overexpressed human cancer genes (2010, background): “Analogous in vitro knockdown experiments can also be undertaken using drugs that target a gene or its encoded protein, as demonstrated by drugs that target MET and only inhibit the growth of gastric cancer cell lines containing the 7q31 amplicon that includes MET”
Strategies and challenges for the next generation of therapeutic antibodies (2010, background): “As a common feature, a tumour must be fully dependent on the antibody target for the therapeutic antibody to affect growt”