Pediatric patients with B-cell acute lymphoblastic leukemia (B-ALL)—a cancer of the blood and bone marrow —can sometimes relapse with features of both B-ALL and a different type of blood cancer, acute myeloid leukemia (AML). In a study published in Nature Cancer, UHN’s Dr. John Dick at Princess Margaret Cancer Centre and Dr. Charles Mullighan at St. Jude Children’s Research Hospital investigated the ability of cells to change from one type to another in B-ALL, and how it affects treatment response.
B-ALL is characterized by the abnormal proliferation of immature lymphoid cells—immune cells that develop into specific types of white blood cells, such as B lymphocytes (B-cells). Categorizing patients into B-ALL subtypes and identifying associated risk levels can predict treatment response and likelihood of relapse. Although pediatric B-ALL cure rates have improved, high-risk children still face poor outcomes, and relapse remains a major cause of death.
Evidence suggests that B-ALL can switch from lymphoid to myeloid lineages after certain immunotherapies or chemotherapy. This phenomenon occurs when a cancerous cell originally classified as lymphoid (e.g., a B-cell precursor) transforms into a myeloid-like cell, such as a granulocyte or macrophage precursor. Malignancies in these lineages lead to different blood cancers, such as ALL from lymphoid cells and AML from myeloid cells. ALL and AML have different molecular features and require different treatment targets.
These findings underscore the importance of understanding B-cell development and lineage switching to predict treatment response. To achieve this, the team analyzed the active and expressed genes (i.e., the transcriptome) of individual leukemia cells from 89 B-ALL patient samples and compared them to normal human B-cell development. To do this, they developed the first comprehensive single-cell reference atlas of normal human B-cell development, spanning over 100,000 cells from various tissue sources.
In constructing this atlas, they discovered that a population of stem cells previously thought to only be capable of producing lymphoid cells (such as B cells) had the hidden ability to produce myeloid cells in the experimental setting.
The researchers found that some B-ALL patient samples contained leukemia cells that highly resemble this population of stem cells with myeloid potential. B-ALL patients who had more of these specific leukemia cells were also more likely to have genomic alterations associated with lineage shifts from lymphoid leukemia to myeloid leukemia at disease relapse.
“Some of these immature lymphoid cells can still develop into myeloid cells,” says Dr. Dick, Senior Scientist at the Princess Margaret Cancer Centre. “This ability, called multipotency, may explain the transition from ALL cases to AML in response to B-cell-specific immunotherapy.”
"We developed a Multipotency Score to describe the abundance of multipotent leukemic cells in patient samples. This score can help predict clinical outcomes,” says Dr. Andy Zeng, co-first author of the study. When tested in independent B-ALL patient datasets, a higher Multipotency Score was associated with higher-risk disease and older age. A high score in pediatric patients was also found to be linked to chemo-resistance and worse overall survival.
“Our research advances our understanding of normal and cancerous B-cell development, which may ultimately enhance risk stratification and therapy development for B-ALL patients,” says Dr. Mullighan, co-corresponding author of the study.
Dr. John Dick, Senior Scientist at Princess Margaret Cancer Centre (PM) and Professor of Molecular Genetics at the University of Toronto (U of T) is a co-senior author of the study. Dr. Dick is also the Helga and Antonio De Gasperis Chair in Blood Cancer Stem Cell Research.
Dr. Charles Mullighan, Co-leader of the Hematological Malignancies Program of the St. Jude Comprehensive Cancer Center is co-senior author of the study.
The co-first authors of the study are Dr. Ilaria Iacobucci, Staff Scientist at St. Jude Children’s Hospital; Dr. Andy Zeng, MD/PhD Candidate at PM and the Temerty Faculty of Medicine at U of T and recent Doctoral Graduate; Dr. Qingsong Gao, Research Scientist at St. Jude Children’s Hospital; and Dr. Laura Garcia-Prat, former Postdoctoral Researcher at UHN and currently a Senior Scientist at Cimeio Therapeutics.
This work was supported by The Princess Margaret Cancer Foundation, St. Jude Children's Research Hospital - ALSAC, the Canadian Institutes of Health Research, National Cancer Institute, Ontario Institute for Cancer Research, International Development Research Centre, Canadian Cancer Society, Terry Fox Research Institute, University of Toronto, University of Toronto’s Medicine by Design, Ontario Government, Alex’s Lemonade Stand Foundation, St. Baldrick's Foundation, Southwest Oncology Group National Clinical Trials Network, and the Henry Schueler 41&9 Foundation.
Ilaria Iacobucci reported consultation honoraria from Arima and travel expenses from Mission Bio and Takara. Charles G. Mullighan received research funding from AbbVie and Pfizer, honoraria from Amgen and Illumina, and royalty payments from Cyrus. He is on an advisory board for Illumina. John E. Dick received research funding from BMS/Celgene and IP licenses from Pfizer/Trillium Therapeutics. For other competing interests, see the manuscript.
Iacobucci I, Zeng AGX, Gao Q, Garcia-Prat L, Baviskar P, Shah S, Murison A, Voisin V, Chan-Seng-Yue M, Cheng C, Qu C, Bailey C, Lear M, Witkowski MT, Zhou X, Zaldivar Peraza A, Gangwani K, Advani AS, Luger SM, Litzow MR, Rowe JM, Paietta EM, Stock W, Dick JE, Mullighan CG. Multipotent lineage potential in B cell acute lymphoblastic leukemia is associated with distinct cellular origins and clinical features. Nat Cancer. 2025 Jun 27. doi: 10.1038/s43018-025-00987-2
Atherosclerosis—the buildup of cholesterol (called plaques) and inflammation in artery walls—is a leading cause of heart disease and stroke. Researchers at UHN, led by Dr. Kathryn Howe, are studying how the endothelium—the thin layer of cells lining blood vessels—helps drive this process. The team developed the first experimental model to track how endothelial cells (ECs) communicate in organisms and identified EC communication signals that drive carotid artery plaque instability.
ECs help regulate inflammation and blood flow by releasing tiny particles called extracellular vesicles (EVs). These EVs carry messages in the form of proteins, fats, and genetic material. This dynamic cell-to-cell communication may help drive both plaque development and its sudden complications, such as heart attack or stroke.
However, little is known about these EVs’ biological cargo, their cellular origin or destination, and their functional roles in human plaque formation. In addition, tracking EV transfer from ECs in real time remains challenging. Two studies from Dr. Howe’s team delve into these issues and work to overcome these limitations.
In a study in the journal Circulation Research, the team generated a new preclinical model that uses a glowing green marker to follow EC-derived EVs in real time. This offers a powerful new way to track how EVs move and act within blood vessels—especially in developing plaques—providing a tool for studying EC-driven conditions such as stroke, heart failure, diabetes, cancer metastasis, and aging.
In a second study, published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, the team analyzed EVs from human carotid artery plaques—where plaque buildup in neck arteries can lead to stroke. In addition to impeding blood flow, the plaques can also become unstable and rupture, releasing material that obstructs an artery and leads to a heart attack or stroke.
The team examined EVs from human carotid plaques, comparing samples from patients with and without symptoms of stroke. Using RNA sequencing and protein analysis, they examined EV cargo and traced their origins and destinations. They found more EVs in plaques than in surrounding tissue—especially in symptomatic patients. These EVs carried different microRNAs and proteins depending on whether plaques were stable or prone to rupture.
In symptomatic plaques, EVs showed more complex communication with nearby cells, particularly endothelial cells, and appeared to promote new blood vessel growth—a process linked to plaque instability.
These findings suggest that EVs help drive disease progression and could be targets for new treatments to prevent stroke and other cardiovascular events. Together, these studies highlight EVs as important drivers of atherosclerosis and introduce a new model to study their role.
For the Circulation Research study:
Mandy Kunze Guo, Doctoral Candidate at UHN and the Institute of Medical Science at the University of Toronto, is the first author of the study.
For the Arteriosclerosis, Thrombosis, and Vascular Biology study:
Dr. Sneha Raju, Medical Resident and recent Doctoral graduate from UHN and the Institute of Medical Science at the University of Toronto, is the first author of the study.
Dr. Kathryn L. Howe, Scientist at the Toronto General Hospital Research Institute (TGHRI) and Associate Professor in the Department of Surgery at the University of Toronto, is the corresponding author for both studies.
Co-author Dr. Jason Fish, Senior Scientist at TGHRI, collaborates extensively with Dr. Howe and together, they co-supervise several graduate students, including those involved in this research. To see more about their laboratories, see https://howeandfishlabs.com.
Dr. Howe holds the Blair Early Career Professorship in Vascular Surgery (University of Toronto) and is supported by the Canadian Institutes of Health Research (CIHR), the Heart and Stroke Foundation of Canada, Wylie Scholar Award from Vascular Cures (2020-2023), the University of Toronto, Peter Munk Cardiac Centre, and the UHN Foundation.
For a more comprehensive list of funding and list of competing interests, see the manuscripts.
Raju S, Turner ME, Cao C, Abdul-Samad M, Punwasi N, Blaser MC, Cahalane RME, Botts SR, Prajapati K, Patel S, Wu R, Gustafson D, Galant NJ, Fiddes L, Chemaly M, Hedin U, Matic L, Seidman MA, Subasri V, Singh SA, Aikawa E, Fish JE, Howe KL. Multiomic Landscape of Extracellular Vesicles in Human Carotid Atherosclerotic Plaque Reveals Endothelial Communication Networks. Arterioscler Thromb Vasc Biol. 2025 May 29. doi: 10.1161/ATVBAHA.124.322324.
Guo MK, Scipione CA, Breda LCD, Prajapati K, Raju S, Botts SR, Abdul-Samad M, Patel S, Yu G, Dudley AC, Fish JE, Howe KL. Tracking Endothelial Extracellular Vesicles in a Mouse Model of Atherosclerosis. Circ Res. 2025 Jun 6;136(12):1629-1631. doi: 10.1161/CIRCRESAHA.124.326024. Epub 2025 Apr 23. PMID: 40265255; PMCID: PMC12136386.
On June 12, 2025, more than 250 in-person attendees—and over 120 virtual participants—gathered at Toronto’s MaRS Discovery District to celebrate the launch of UHN’s newest research collaborative centre: the Collaborative Centre for Immunology to Immunotherapy (Ci2i). The inaugural Ci2i Symposium brought together leading experts in immunology, cell therapy, virology, and immunotherapy for a day of networking, scientific dialogue, and learning.
The event opened with Drs. Tracy McGaha, Chair of the Ci2i Symposium Planning Committee, Brad Wouters, Executive Vice President of Science and Research at UHN, and Pam Ohashi, Chair of Ci2i. Dr. McGaha took the stage first to welcome attendees and set the tone for an exciting day ahead, followed by Drs. Wouters and Ohashi who spoke about the significance of the centre’s launch and shared their vision for the future of immune-related research at UHN.
Throughout the day, researchers from the University of Toronto and UHN presented their work, highlighting the breadth and depth of ongoing research in immunology, virology, immunotherapy, and related fields. Attendees were encouraged to ask questions and engage in thoughtful discussions with the presenters.
Presenters from UHN’s Toronto General Hospital Research Institute included:
● Dr. Brian Coburn, Senior Scientist
● Dr. Slava Epelman, Senior Scientist
● Dr. Stephen Juvet, Scientist
● Dr. Sonya MacParland, Senior Scientist
Presenters from UHN’s Princess Margaret Cancer Centre included:
● Dr. Naoto Hirano, Senior Scientist
● Dr. Tracy McGaha, Senior Scientist
● Dr. Linh Nguyen, Head, Centre for Cell Manufacturing
● Dr. Trevor Pugh, Senior Scientist
● Dr. Ben Wang, Head, Centre for Integrative Immune Analysis
Other presenters a part of TeamUHN included:
● Dr. Gideon Hirschfield, Director, Autoimmune Liver Disease Program, Francis Family Liver Clinic and Toronto Centre for Liver Disease
● Dr. Elmar Jaeckel, Medical Director, Ajmera Transplant Centre
Presenters from the Department of Immunology at the University of Toronto included:
● Dr. Dana Philpott, Associate Chair, Research
● Dr. Alberto Martin, Professor
● Dr. Jennifer Gommerman, Professor
Two international keynote speakers—Dr. Huji Xu, from Shanghai Changzheng Hospital, and Dr. Donna Farber, from Columbia University—bookended the day’s presentations. These internationally recognized researchers provided a global perspective on immune science, showcased their field-defining work, and applauded the Ci2i for its focus on innovation and collaboration.
The symposium also featured a powerful talk by Charlotte Grad, a Ci2i patient partner and former stage 4 non-Hodgkin lymphoma patient treated at the Princess Margaret Cancer Centre. As a CAR-T cell therapy recipient, Charlotte shared her journey, reminding the audience of the real-world impact of immune-based research. “I am here today because of you,” she said to a captivated audience. Her story underscored the life-changing impact that immunology and immunotherapy research at UHN has—and will continue to have with the establishment of the Ci2i.
Ci2i extends its sincere thanks to everyone who helped make the day such a success. This includes the Ci2i Symposium Planning Committee, Firdaus Bakharia, Sara Lamorte, and Ci2i Project Manager Ksenia Meteleva; Dr. Tracy McGaha, Chair of the Ci2i Symposium Planning Committee; Drs. Robert Inman and Naoto Hirano, Co-Chairs of Ci2i; Pam Ohashi, Chair of Ci2i; the Ci2i Executive Committee; and the many volunteers.
The Ci2i team also thanks the Symposium’s five sponsors and three exhibitors:
● Title Presentation Sponsor: 10x Genomics
● Morning Keynote Speaker Sponsor: CDD Vault
● Evening Presentation Sponsors: Bio-Rad Laboratories, and Sanofi
● Patient Partner Sponsor: Cytek Biosciences
● Exhibitors: STEMCELL Technologies, Miltenyi Biotech, and Olink
Abdominal aortic aneurysms (AAAs) are a silent but deadly threat and a leading cause of death in men over 65 in Canada. Currently, there are no treatments to prevent the growth and rupture of these aneurysms. New research from UHN has uncovered how AAAs form and the impact of smoking, potentially opening the door to targeted treatments.
Although initially asymptomatic, AAAs are defined as a swelling of the abdominal aorta—the portion of the aorta that carries blood from the heart to the abdomen. Progressive weakening and dilatation (being stretched or widened) of the vessel wall make it more likely to rupture, which is a surgical emergency and results in death in 50% to 85% of patients. There is limited understanding of how AAAs form and how risk factors such as smoking and arterial plaque buildup contribute to clinical outcomes.
A team led by UHN’s Dr. Clinton Robbins and collaborators used pre-clinical lab models to mimic these risk factors: cigarette smoke exposure and high cholesterol. They found that cigarette smoke drove aneurysm formation by damaging the cells that line the aorta.
Genetic sequencing techniques revealed that this damage triggered inflammation and caused immune cells called macrophages to gather within arterial plaque, where they release enzymes that degrade the elastic fibres of the aortic wall—eventually causing it to expand and rupture like a balloon.
The study also identified a specific type of inflammatory macrophage that was consistent across both pre-clinical lab models and humans, and was central to this destructive process.
“This research sheds light on how smoking worsens AAA and pinpoints the immune cells behind the destruction,” says Dr. Clinton Robbins, Senior Scientist at Toronto General Hospital Research Institute. “It could open the door to new treatments that target these harmful pathways—potentially stopping aneurysms before they burst and become fatal.”
Co-first authors of the study include: Dr. Danya Thayaparan, former Postdoctoral Researcher at McMaster University and current Scientific Advisor at GSK; Dr. Takuo Emoto, Researcher at Kobe University Graduate School of Medicine and former Postdoctoral Researcher at Toronto General Hospital Research Institute (TGHRI); Dr. Aniqa B. Khan, Doctoral Candidate at TGHRI; Dr. Rickvinder Besla, former Doctoral Student at TGHRI and current Senior Scientist at Merck; Dr. Mahmoud El-Maklizi, Postdoctoral Researcher at TGHRI; and Homaira Hamidzada, Doctoral Student at TGHRI.
Drs. Emoto and Khan are also co-corresponding authors on the paper.
Dr. Ken-ichi Hirata, Researcher at Kobe University and Dr. Martin R. Stampfli, Professor at McMaster University, are co-senior authors of the study.
Dr. Clinton S. Robbins, Senior Scientist at Toronto General Hospital Research Institute and Associate Professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, is a co-corresponding and co-senior author of the study. Dr. Robbins is a Tier 1 Canada Research Chair in Cardiovascular Immunology and the Peter Munk Chair in Aortic Disease Research at the University Health Network.
This work was supported by the Canadian Institutes of Health Research, the Flight Attendants Medical Research Institute, the Japan Society for the Promotion of Science, the Japan Agency for Medical Research and Development, the MSD Life Science Foundation, the Japan Foundation for Applied Enzymology; and the Naito Foundation, University of Toronto’s Medicine by Design, and the Government of Canada, and UHN Foundation.
Thayaparan D, Emoto T, Khan AB, Besla R, Hamidzada H, El-Maklizi M, Sivasubramaniyam T, Vohra S, Hagerman A, Nejat S, Needham-Robbins CE, Wang T, Lindquist M, Botts SR, Schroer SA, Taniguchi M, Inoue T, Yamanaka K, Cui H, Al-Chami E, Zhang H, Althagafi MG, Michalski A, McGrath JJC, Cass SP, Luong D, Suzuki Y, Li A, Abow A, Heo R, Pacheco S, Chen E, Chiu F, Byrne J, Furuyashiki T, Husain M, Libby P, Okada K, Howe KL, Heximer SP, Yamashita T, Wang B, Rubin BB, Cybulsky MI, Roy J, Williams JW, Crome SQ, Epelman S, Hirata KI, Stampfli MR, Robbins CS. Endothelial dysfunction drives atherosclerotic plaque macrophage-dependent abdominal aortic aneurysm formation. Nat Immunol. 2025 May;26(5):706-721. doi: 10.1038/s41590-025-02132-8.
The Stem Cell Network, together with partner organizations, has committed $33 million to advance Canadian stem cell and regenerative medicine research and clinical trials. As part of this national investment, UHN researchers were awarded $3.1 million across seven projects, including three led by UHN principal investigators.
The following UHN-led teams received funding to support innovative stem cell research in heart regeneration, the development of biological pacemakers, and cystic fibrosis:
Dr. Michael Laflamme | Impact Award
The Impact Award supports proof-of-principle experiments, including the development of novel therapeutic or technical approaches to advance regenerative medicine therapies. This award supports Dr. Laflamme, Senior Scientist at the McEwen Stem Cell Institute, with his project entitled: “RNA-based strategies to promote the engraftment of stem cell-derived cardiomyocytes”. UHN co-investigators include Drs. Bowen Li and Terrence Yau.
Dr. Stephanie Protze | Early Career Researcher Jump Start Award
The Early Career Researcher Jump Start Award supports early-career investigators in establishing research programs focused on regenerative medicine. This award supports Dr. Protze, Scientist at the McEwen Stem Cell Institute, with her project entitled: “Developing a stem cell-based conduction bridge for patients with atrioventricular block”. UHN co-investigators include Drs. Michael Laflamme, Gary Bader, and Sara Vasconcelos.
Dr. Bowen Li | Early Career Researcher Jump Start Award
Dr. Li, Affiliate Scientist at the Princess Margaret Cancer Centre, also received an Early Career Researcher Jump Start Award to support his project entitled: “Nonviral delivery of prime editors for gene therapy of cystic fibrosis”.
UHN researchers also received funding as co-investigators on four projects led by collaborating institutions. These include research focused on advanced therapies for lung and heart disease. UHN researchers on these teams include Drs. Cindi Morshead, Guillaume Richard-Carpentier, Bowen Li, Milica Radisic, and Michael Laflamme.
Congratulations to all UHN researchers who received SCN funding. To view all the funded projects and for additional information, visit the Stem Cell Network’s competition results page.
Researchers at UHN reveal how a molecule known as circular RNA (circRNA) drives the transformation of specific prostate and lung cancers into more aggressive, treatment-resistant forms, highlighting new potential therapeutic targets.
Prostate and lung adenocarcinomas are cancers that form in glands that line these organs. Interference of gene regulatory programs in neurons can transform these cancers into more aggressive types: neuroendocrine prostate cancer (NEPC) and small cell lung cancer (SCLC), respectively. Both NEPC and SCLC are neuroendocrine tumours, forming from neuroendocrine cells—nerve cells that also produce hormones. NEPC and SCLC are more difficult to treat and share similar genetic changes.
CircRNAs are a form of RNA, genetic material that generally does not produce proteins but instead helps regulate gene activity. Previous evidence has identified a link between circRNAs and the regulation of various biological processes important for cancer development. However, their role in driving cancer transformation remains unexplored.
Through gene expression analysis, a research team from the Princess Margaret Cancer Centre identified a specific circRNA, circRMST, which is highly active in NEPC and SCLC. They found that circRMST is essential for tumour growth and the expression of ASCL1—a key regulator for turning a cell into a neuroendocrine cell.
Using genetic tools in experimental models, the research team found that circRMST is also essential for the transformation of adenocarcinoma into aggressive neuroendocrine tumour types. Further analysis revealed that circRMST interacts with two other key proteins, SOX2 and NKX2-1, to promote ASCL1 expression and drive the development of neuroendocrine cell characteristics.
This research underscores the direct regulatory role of circRMST in the progression of prostate and lung adenocarcinoma. By highlighting an essential player in the changes of these cancers, the findings reveal potential new insights into therapeutic strategies for targeting neuroendocrine tumours.
Dr. Mona Teng, a former doctoral student at Princess Margaret Cancer Centre (PM) is the co-first author of the study.
Jiacheng Guo from the Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai, China, is the co-first author of the study.
Dr. Xin Xu, a Postdoctoral Researcher at PM, is the co-first author of the study.
Dr. Housheng (Hansen) He, a Senior Scientist at PM, and Professor in the Department of Medical Biophysics at the University of Toronto is the lead corresponding author of the study.
Dr. Himisha Beltran, Associate Professor of Medicine at Dana Farber Cancer Institute and Harvard Medical School is a co-corresponding author of the study.
Dr. Jun Quin, Professor and Principal Investigator at the Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, is a co-corresponding author of the study.
This work was supported by the Canadian Institutes of Health Research, the Terry Fox Research Institute, the Marathon of Hope Cancer Centres Network, the Joey and Toby Tanenbaum/Brazilian Ball Chair in Prostate Cancer at Princess Margaret Cancer Centre, the Canada Foundation for Innovation, Cancer Research Society, National Institutes of Health/National Cancer Institute, the Clinical and Translational Science Center at Weill Cornell Medical Center, National Natural Science Foundation of China, Prostate Cancer Foundation (PCF) and the United States Department of Defense.
Dr. Housheng (Hansen) He is a Tier 1 Canada Research Chair in RNA Medicine.
Co-author Dr. Benjamin Lok reports grants from Pfizer; and grants, personal fees, and non-financial support from AstraZeneca outside the submitted work.
Teng M, Guo J, Xu X, Ci X, Mo Y, Kohen Y, Ni Z, Chen S, Guo WY, Bakht M, Ku S, Sigouros M, Luo W, Macarios CM, Xia Z, Chen M, Ul Haq S, Yang W, Berlin A, van der Kwast T, Ellis L, Zoubeidi A, Zheng G, Ming J, Wang Y, Cui H, Lok BH, Raught B, Beltran H, Qin J, He HH. Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation. Cancer Cell. 2025 May 12. doi: 10.1016/j.ccell.2025.03.027. Epub 2025 Apr 17.
For Dr. Lisa Boivin, a member of the Deninu Kųę́ First Nation in Denendeh (Northwest Territories) and an Indigenous Educator, making art is more than an act of creative expression. It is a chance to share knowledge in the way her ancestors have for centuries and help people understand the importance of cultural safety and Indigenous Peoples’ experiences in health care and research.
On Wednesday, May 28, members of the UHN community gathered in the De Gasperis Conservatory at Toronto General Hospital for an Arts-Based Education Open House to learn more about how Lisa educates through art. The afternoon promised a taste of the workshops Lisa hosts for UHN and Indigenous Peoples in the city.
Participants were encouraged to create their own artwork, leave their mark in the guestbook, and add to a large group collage. The space was filled with laughter, thoughtful conversations, and moments of connection as people explored their creativity together. Lisa shared the meanings behind the animals in the collage, explaining the important lessons they carry in Indigenous knowledge.
Throughout the afternoon, laughter and thoughtful conversation filled the air as participants’ creativity flourished, and Lisa shared Indigenous teachings on what people can learn from the various animals that were included in the collage.
Several of Lisa’s artworks were also on display at the event, including a print of her work entitled Unravelling the Whispers of Ancestors, which was raffled to one lucky attendee. Other winners took home copies of Lisa’s books: I Will See You Again and I Dream Medicine Dreams.
Events like this Open House bring the UHN community one step closer to decolonizing research and health care spaces. Centering the voices, teachings, and experiences of Indigenous communities is the first step toward ensuring research at UHN reflects their needs, but it is certainly not the last. With the help of incredible members of the community like Dr. Lisa Boivin, UHN is committed to the continued learning and work necessary to make UHN spaces safe for and welcoming to Indigenous Peoples.
The UHN community thanks all those who helped make this event such a success, including the UHN Research IDEA team.
To learn more about Lisa and her work, read her You @TeamUHN feature here.
To find out more about or book one of Lisa’s workshops, email Lisa at lisa.boivin@uhn.ca.
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