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Poul Sorensen


UBC, BC Cancer Research Institute

Dr. Sorensen received his Ph.D. and MD from the University of British Columbia (UBC) and McGill University. He completed his postdoctoral training at the University of Minnesota, Minneapolis and Children’s Hospital Los Angeles, University of Southern California. Dr. Sorensen is a professor of Pathology and Laboratory Medicine at University of British Columbia and he is also a distinguished scientist at the BC Cancer Research Institute. He holds the Asa and Kashmir Johal Chair in Childhood Cancer Research at UBC.

Why do you study metabolism?

We predict/hypothesize that pediatric cancer cells have various metabolic vulnerabilities that are not seen at the genomic level. That is why we are looking at these cells using proteomics and metabolomics tools.

Why it fascinates you?

You would think that cancer cells could readily survive the metastatic process such as entering the bloodstream, but it is in fact a harsh environment, and we are currently deciphering the mechanisms used by pediatric cancer cells to adapt and survive in these stressful conditions. We hypothesize that dealing with metabolic stress is one of these mechanisms.

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Research Focus

Identifying targetable tumour specific pathways

We are interested in identifying targetable metabolic pathways altered in childhood cancer cells. We think that cancer cells able to adapt to stresses have higher metastatic capacity. We have uncovered a number of these proteins (e.g. IL1RAP, STEAP1/2) and are working to develop immunotherapies directed against these targets.

Adaptation to oxidative stress

Cancer cells are thought to require higher metabolic capacity and under stress can adapt many cellular processes such as mRNA translation to meet metabolic needs. We showed that selective mRNA translation by childhood cancer cells allows them to adapt to diverse acute tumor microenvironment stresses. Some of the proteins we study (e.g. YB1, G3BP1, eIF4A, and IL1RAP) are known to drive the selective translation of antioxidant factors and maintain cysteine and glutathione pools, thereby blocking ferroptosis.

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