LAUSR

The heterogeneity of tumor cells underlies acquired drug resistance to a variety of therapeutic approaches. The advent of next-generation sequencing has facilitated a wave of studies identifying genetic mutations, which may be preexisting or acquired during treatment, that drive drug resistance and tumor relapse. However, it has recently become clear that non-mutational mechanisms of drug resistance, such as cell state switching from an epithelial to mesenchymal state, can also play an important role in the process of acquired drug resistance. Non-mutational drug resistance is relatively poorly understood and represents fertile ground for the discovery of novel therapeutic targets. Drug-tolerant “persister” cells are an experimental model of non-mutational cancer drug resistance in which small fractions ( Citation Format: Matthew J. Hangauer, Vasanthi S. Viswanathan, Matthew J. Ryan, Dhruv Bole, John K. Eaton, Alexandre Matov, Jacqueline Galeas, Harshil D. Dhruv, Michael E. Berens, Stuart L. Schreiber, Frank McCormick, Michael T. McManus. GPX4 is a broadly shared gene vulnerability among residual tumors [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2017 Oct 26-30; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2018;17(1 Suppl):Abstract nr B098.