Abstract 5439: Metabolomic study of EGFR drug resistance mechanisms

Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA Therapies targeting EGFR often fail after certain period of treatment due to development of resistance. There are many causes of resistance such as genetic mutations of KRAS, BRAF, etc.. Overexpression of other receptor tyrosine kinases can also lead to resistance of EGFR therapies. A therapeutic targeting metabolic phenotypes that can overcome multiple resistance mechanisms is highly desired. In order to identify the Achilles heel of resistant cell metabolism, we investigated the metabolic effects of the current EGFR targeting agents as well as the metabolic differences between sensitive and resistant cancer cells. Citation Format: Yang Zhao, Bo Tan, Ming-Shang Kuo, Ling Liu, Matthew D. Breyer. Metabolomic study of EGFR drug resistance mechanisms. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5439. doi:10.1158/1538-7445.AM2014-5439