Breakthrough T1D Canada is excited to continue its successful partnership with the Canadian Islet Research and Training Network (CIRTN) and announce a fourth cohort of co-funded trainees beginning in 2026.
CIRTN was established in 2020 as a world-class training and research network with joint contributions from the University of Alberta, University of British Columbia, University of Manitoba, Université de Montréal, Institut de Recherches Cliniques de Montréal, and the University of Toronto and now includes 12 institutions from across Canada.
Breakthrough T1D Canada has partnered with CIRTN to leverage funding to this network from the National Science and Engineering Research Council – Collaborative Research and Training Experience (NSERC-CREATE) program.
Previous cohorts:
Dr. Austin Miller –Postdoctoral Fellow (supervisor: Francis Lynn, University of British Columbia)
Improving the ability to generate stem cell-derived pancreatic islets in the lab
Regenerative medicine approaches are being developed as an alternative in which pancreatic islets are transplanted into patients to restore autonomous insulin secretion, reducing the patient burden of T1D management. Stem cell-derived pancreatic islets (stem cell islets) have the potential to provide an unlimited supply of islets for transplantation.
Overall, my research aims to improve our ability to generate stem cell-derived islets in the lab. I will develop tools to study cellular pathways that allow cells to manage the burden of secreting proteins like insulin and perform studies to better understand the role of these pathways in the generation of insulin-secreting cells. These findings will inform strategies to further improve the efficiency of stem cell-derived islet generation.
Dr. Chris Schaaf – Postdoctoral Fellow (supervisor: Patrick MacDonald, University of Alberta)
Standardizing stem cell-derived beta cells
The advent of stem cells has provided a promising approach towards generating a functional cure for type 1 diabetes. However, current protocols do not generate stem cell-derived beta cells that appropriately produce and regulate insulin secretion, and there is a lack of standardized assays, benchmarks, and analytical tools for comparing stem cell-derived beta cells to human donor islets.
This project will leverage the humanislets.com dataset – a collection of ‘gold standard’ molecular and functional datasets from hundreds of human organ donors – funded by Breakthrough T1D and CIHR. Using this robust dataset and collaborative expertise in computation and artificial intelligence, we will perform comparative analyses and benchmarking for the improvement of stem cell-derived beta cell outcomes. This will enable us to develop benchmarking standards and protocols that can be used by researchers anywhere in the world to compare their own lab generated stem cell-derived beta cells to our repository of human donor islets data, and use that data to generate stem cell-derived beta cells that truly mimic the function of human beta cells.
Yihan Luo – PhD student (supervisor: Kacey Prentice, University of Toronto)
A new approach to prevent type 1 diabetes by strengthening insulin producing cells
In the human body, organs communicate with each other through hormones, such as insulin, made by beta cells in the pancreas. Insulin tells fat, muscle, and liver cells to absorb sugar from the blood, which provides energy and keeps blood sugar levels in balance. In type 1 diabetes (T1D), the immune system destroys beta cells, causing lifelong insulin deficiency. Evidence suggests that T1D begins before beta cell loss, due to disrupted insulin responses and organ–pancreas communication. Fabkin, a hormone complex secreted by fat, affects beta cell health and research has shown that blocking it in mice helped beta cells stay healthier. Our project studies Fabkin’s key component, NDPK, to learn how it affects beta cell survival and function, and test whether NDPK-targeting drugs can prevent or delay T1D. If successful, this work could lay the foundation for a new approach to prevent T1D by protecting beta cells before they are damaged or lost.
