Abstract 1500 Identification of Druggable and Redox Vulnerabilities in Cancer

Multiple anticancer drugs have been proposed to cause cell death, in part, by increasing the steady-state levels of cellular reactive oxygen species (ROS). However, for most of these drugs exactly how the resultant ROS function and are sensed is poorly understood. It remains unclear which proteins the ROS modify and their roles in drug sensitivity/resistance. To answer these questions, we examined 11 anticancer drugs with an integrated proteogenomic approach identifying many unique targets but also shared ones–including ribosomal components, suggesting common mechanisms by which drugs regulate translation.