Abstract
Background
Efficient DNA repair in response to standard chemo and radiation therapies often contributes to GBM therapy resistance. Understanding the mechanisms of therapy resistance and identifying the drugs that enhance the therapeutic efficacy of standard therapies may extend the survival of GBM patients. In this study, we investigated the role of KDM1A/LSD1 in DNA double-strand break (DSB) repair and a combination of KDM1A inhibitor and TMZ in vitro and in vivo using patient-derived GSCs.