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. In particular, using a novel genetically modified mouse model, I will show that FH loss has different outcomes in different tissues, and whilst kidneys are very robust to FH loss, other tissues don’t tolerate FH loss and here FH-deficient cells are negatively selected. Our work provides some insights into potential mechanisms of tissue-specific tumorigenesis based on metabolic permissiveness.

Zoom-Meeting-Link

Meeting-ID: 672 2119 5153
Code: 721518