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EGFR and c-Met Inhibitors are Effective in Reducing Tumorigenicity in Cancer

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journal contribution
posted on 29.08.2016 by Amanda Stone, Kymberly Harrington, Mark Frakes, Kory Blank, Supriya Rajanna, Ichwaku Rastogi, Neelu Puri
EGFR and c-Met are receptor tyrosine kinases that are implicated in tumor development and progression in several types of cancer. Both EGFR and c-Met, which are known to be overexpressed and mutated in cancer, share common signaling pathways, including the PI3K/ Akt and MAPK pathways. Small molecule tyrosine kinase inhibitors and monoclonal antibodies that work against EGFR and c-Met are at the forefront of cancer therapy, but their individual efficacies are limited due to the development of drug resistance. In recent pre-clinical studies, we observed that combination therapy using mTOR and Wnt inhibitors with EGFR or c-Met tyrosine kinase inhibitors resulted in overcoming drug resistance. Our studies also indicated that EGFR and c-Met tyrosine kinase inhibitor resistance may be due to activation of alternative signaling pathways. The development of additional combinatorial therapies is underway, and various combinations of inhibitors have shown promising results in clinical trials. Future studies in this direction could be the basis for development of new cancer therapeutics, utilizing EGFR and c-Met inhibitors, which could greatly improve patient prognosis.

History

Publisher Statement

This is a copy of an article published in the Journal of Carcinogenesis and Mutagenesis. © 2014 Stone A, et al.

Publisher

OMICS International

Language

en_US

Issue date

05/05/2014

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