Acute myeloid leukemia (AML) is notoriously difficult to treat. Only 28 percent of patients survive beyond 5 years after diagnosis. Mitophagy, a process in which damaged mitochondria are eliminated to prevent the transmission of death signals, has been identified as a key mechanism that allows leukemia cells to resist the effects of the widely prescribed drug venetoclax, according to a recent study published in Cancer Discovery and led by scientists from Perlmutter Cancer Center at NYU Langone Health.

Today on OncTimes Talk, we interview Dr. Christina Glytsou, lead author of the study, and discuss the reasons behind leukemia cells’ resistance to venetoclax, a BH3 mimetic drug that promotes cancer cell death in individuals with AML. Dr. Glytsou holds a joint appointment as an Assistant Professor in the Department of Chemical Biology at the Ernest Mario School of Pharmacy of Rutgers University and the Department of Pediatrics at Rutgers Robert Wood Johnson Medical School. She is a member of Cancer Metabolism & Immunology and the Cancer Pharmacology Programs, at the Cancer Institute of New Jersey. Dr. Glytsou’s laboratory aims to address fundamental questions unravelling the role of mitochondrial biology in blood malignancies’ progression and drug resistance.