The role of mitochondrial dysfunction in cancer has been debated for over a century. Recent bioinformatic data analyses revealed that mitochondrial genes are suppressed in cancer with poor clinical outcome. Furthermore, the fact that mutations of core metabolic enzymes in the mitochondria such as Fumarate Hydratase (FH) cause renal cancer strongly indicates that mitochondrial dysfunction can drive cancer. Today, I will provide an overview of our recent findings about the molecular mechanisms through which mitochondrial dysfunction can drive transformation and shape cancer progression, focusing on FH loss. Our work provides some insights into potential mechanisms of tumorigenesis caused by the accumulation of fumarate, a bona fide oncometabolite.
8 Maggio 2020, ore 12, online
Dr. Christian Frezza - MRC Cancer Unit, Cambridge Cancer Center, at the University of Cambridge, UKhttps://meet.google.com/gbs-swyw-hxp