Logo Rosalind & Morris Goodman Cancer Institute

Nov 10, 2025
From 12 PM to 1 PM

Location ABCanada

"Mitochondrial DNA mutations in cancer: prevalent and relevant”" will be presented by Payam Gammage, Ph.D., group Leader at the CRUK Scotland Institute and Professor of Mitochondrial Biology at the University of Glasgow. 

 

GCI Frontiers in Cancer Research Lecture Series

GCI Frontiers in Cancer Research Lecture Series

Mitochondrial DNA mutations in cancer: prevalent and relevant

The Rosalind and Morris Goodman Cancer Institute Frontiers in Cancer Research Lecture Series is pleased to welcome Payam Gammage, Ph.D., Group Leader at the CRUK Scotland Institute and Professor of Mitochondrial Biology at the University of Glasgow.

The seminar will take place on Monday, November 10, 2025 at 12:00pm in the GCI Karp Room 501.


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TBD.


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I am a Group Leader at the CRUK Scotland Institute, Professor of Mitochondrial Biology at the University of Glasgow and an EMBO Young Investigator. My lab is generously supported by CRUK, the ERC and the NIH.

I studied at University College London (MSci, 2011) and the University of Cambridge (PhD, 2015), completing my postdoctoral training in the lab of Prof Michal Minczuk at the MRC Mitochondrial Biology Unit, University of Cambridge. During my time as a trainee, I developed interests in mitochondrial biology, functional genomics, metabolism and cancer, which compelled a move to Glasgow to start my lab at the CRUK Beatson Institute, now Scotland Institute, in 2019.

Since this time work in my lab has focused on somatic mutations in tumor mitochondrial DNA (mtDNA), an understudied class of cancer-associated genetic variant present in half of all tumors. Mutations in mtDNA are an established cause of hereditary metabolic disease in humans, with these patients presenting metabolic phenotypes resembling those often found in cancer cells. Our research aims to explore the mutational landscape of tumor mtDNA, employ functional genomics of mitochondria to explain the role these mutations play in tumor initiation and progression, and exploit vulnerabilities specific to mutant mtDNA tumor phenotypes for patient benefit.