Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence.

ABSTRACT: The relevant role in cancer played by the tyrosine kinase receptor encoded by the MET oncogene led to the development of specific inhibitors, some of which are now in advanced phases of clinical trials. Previous experience has shown that the main limit to the efficacy of most targeted treatments is the advent of resistance. Mechanisms underlying resistance to MET-specific small tyrosine kinase inhibitors (TKIs) have been already described, while nothing is known about resistance to MET monoclonal antibodies, nor about bypassing resistance to chemical TKIs by antibodies or vice-versa. EBC1 lung cancer cells are MET-addicted as a consequence of gene amplification and thus sensitive to MET inhibitors, including the monovalent form of a MET monoclonal antibody (MV-DN30). We generated cells res

SUBMITTER: Martin V 

PROVIDER: S-EPMC5528600 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature