The cancer-causing form of the gene Myc alters the metabolism of mitochondria, the cell’s powerhouse, making it dependent on the amino acid glutamine for survival. In fact, 40 percent of all “hard-to-treat” cancers have a mutation in the Myc gene. Accordingly, depriving cells of glutamine selectively induces programmed cell death in cells overexpressing mutant Myc. Using Myc-active neuroblastoma cancer cells, a team led by Howard Hughes Medical Institute investigator M. Celeste Simon, Ph.D., scientific director for the Abramson Family Cancer Research Institute, Perelman School of Medicine, identified the proteins PUMA, NOXA, and TRB3 as executors of the glutamine-starved cells. These three proteins represent a downstream target in the Myc pathway at which to aim drugs. Roughly 25 percent of all neuroblastoma cases are associated with Myc-active cells.
See more at Penn Medicine