Dr. Christian Frezza is Programme leader at the MRC Cancer Unit, Cambridge Cancer Center, at the University of Cambridge, UK. He studied Medicinal Chemistry at the University of Padova, Italy, and gained his MSc in 2002, after a period of research on mitochondrial toxicity induced by photoactivable anticancer drugs. Christian then joined the laboratory of Luca Scorrano in Padova to start a PhD on mitochondrial dynamics and apoptosis. In 2008, he moved to the Beatson Institute of Cancer Research in Glasgow as recipient of an EMBO Long Term Fellowship, where he investigated the role of mitochondrial defects in tumorigenesis. He moved to the MRC Cancer Unit in 2012 as tenure track Group Leader and became a Programme Leader in 2017. His laboratory is mainly interested in investigating the emerging connection between cancer and metabolism, with a particular focus on mitochondrial metabolism. By using a combination of biochemistry, metabolomics, and systems biology he investigates the role of altered metabolism in cancer with the aim to understand how metabolic transformation regulates the process of tumorigenesis. His aim is to exploit these findings to establish novel therapeutic strategies and diagnostic tools for cancer.
Abstract
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 caused by the loss of FH can drive transformation and shape cancer progression.