Christian Frezza

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The role of mitochondrial dysfunction in cancer has
been debated for over a century. The discovery 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 the 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.

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CECAD
215
Contact: Michael Lässig