The prestigious annual Canada Gairdner Awards recognize the world’s most accomplished researchers whose work is improving our understanding of human health and disease. Since 1957, 426 awards have been given to recipients from over 40 countries. Awardees have advanced our understanding of some of the most important global health and biomedical issues, as well as improved the lives of those living with numerous medical conditions. The recipients of this year’s Canada Gairdner Awards reveal that a full understanding of human disease begins at the most basic level. Here’s how this year’s laureates have affected both the advancement of science and countless human lives. 

Untangling the intricate world of cell communication

Spyros Artavanis-Tsakonas, Iva Greenwald, and Gary Struhl have each been awarded a 2025 Canada Gairdner International Award, which recognizes influential and groundbreaking discoveries in human biology and biomedical science. 

Artavanis-Tsakonas, Greenwald, and Struhl’s pioneering research has provided an understanding of the Notch signaling pathway, which regulates communication between cells during animal development. This communication system is a key player in the development of all living beings. As such, when it goes awry, the effects can result in numerous diseases from cancer to defects of nearly every organ system in our bodies. Understanding how it works, at the most fundamental level, is crucial to fully comprehend how these various diseases work, and importantly, how we might be able to treat them. 

Every animal on Earth contains cells — billions of them, in many cases. As an animal develops, these cells organize into incredibly complex structures such as legs, arms, wings, and tails. Gary Struhl says an easy example of this is butterfly wings. “All butterflies of the same species form wings of the same size, with virtually identical and beautifully complex patterns of colors, stripes, and spots,” says Struhl. For this to happen, cells need to coordinate with neighboring cells and make decisions based on what those cells are doing. “Cells have to be able both to speak and to listen to each other, and just as importantly, they need to change their behavior, including what they are saying, depending on what they are hearing,” says Struhl. The Notch signaling pathway is one way in which this communication happens.

The Notch gene was first discovered over 100 years ago. Since that time, researchers have slowly chipped away at understanding, on a comprehensive level, how it works. Artavanis-Tsakonas, Greenwald, and Struhl have made consequential strides in this area. Significantly, Artavanis-Tsakonas cloned the Drosophila Notch gene. This helped lead to the understanding that Notch is a membrane-bound receptor that interacts with other membrane-bound molecules on adjacent cells. This results in intracellular signaling and permanent shifts in the fate of the cell. 

Greenwald’s work on Notch in nematodes helped establish fundamental properties of the signaling pathway system. Greenwald discovered and cloned the nematode Notch gene LIN-12. This advancement, along with her pioneering genetic studies, helped inform Notch’s role in regulating the fate of a cell and the importance of feedback mechanisms through which the Notch system coordinates the behavior of neighboring cells. Greenwald also discovered that a protein called Presenilin is a core component of the Notch system. It provides the key function of cleaving, or cutting apart, the Notch receptors. 

Then, Struhl and Greenwald performed a series of experiments to better understand and confirm various mechanisms of action through which the Notch signaling system works; specifically, that Notch works as a membrane-tethered transcription factor that is cleaved to release its cytosolic domain (the portion of the Notch receptor that resides inside the cells). The cytosolic domain then enters the nucleus to control gene expression. Finally, using chimeric proteins, Struhl confirmed this cleavage model and showed that ligands exert mechanical force that activates Notch.

This work — by Artavanis-Tsakonas, Greenwald, and Struhl — established Notch as a new paradigm for intercellular signaling. This has enabled researchers to begin to understand its role in both normal animal development and in abnormal development that can lead to various conditions from cancer to developmental abnormalities. “Notch affects almost everything,” says Artavanis-Tsakonas. “Because it affects essentially all cells that are differentiating into something different.” Cancer, as Artavanis-Tsakonas explains it, is one example of a miscommunication amongst cells, which leads to a pathogenic condition. A better understanding of how cells communicate with one another, via the Notch signaling pathway and others, could lead to a new understanding of cancer, and potentially better treatments for it. 

All three scientists credit their enduring interest in the field of cell biology to a lifelong love of genetics. Artavanis -Tsakonas trained as a chemist and was first attracted to genetics as a postdoctoral fellow and never looked back. For Greenwald and Struhl that interest started early, during their undergraduate years. Greenwald says she had long been “fascinated by how a human could be made from a zygote” before she knew what the field of developmental biology was called. Similarly, Struhl recalls an early course he took in college got him hooked on “the awesome power of genetics.”

Significantly altering the natural course of cystic fibrosis 

Michael J. Welsh and Paul Negulescu have each been awarded a 2025 Canada Gairdner International Award, recognizing their pioneering work in uncovering the underlying genetic mutations that cause cystic fibrosis and the subsequent development of life-changing medicines that have radically changed the lives of countless cystic fibrosis patients.

Back in 1989, geneticists Lap-Chee Tsui and Francis Collins, along with their teams, discovered the gene responsible for cystic fibrosis: a protein which they then called cystic fibrosis transmembrane conductance regulator, or CFTR. That discovery, “opened up lots of opportunities to try and understand the cellular and molecular bases of the disease,” says Michael J. Welsh. “As soon as you have a protein, you want to know, what does it do?”

Welsh says he was initially drawn to studying cystic fibrosis by curiosity. “I’m a pulmonary physician, and I was interested in how the lung works,” Welsh says. “I wanted to understand how the lung defends itself from bacteria and other things that we inhale.” He was further inspired to study cystic fibrosis because he was treating patients with the disease. “There was no way to stop their lung disease from progressing. Although we could try our best, we were not treating the real source of the problem. In the lab, I focused on understanding the fundamental defects causing cystic fibrosis, hoping that the knowledge might benefit people with cystic fibrosis.”

Over the course of several years, Welsh and his team uncovered a number of key processes through which the CFTR protein functions and what goes wrong in cystic fibrosis. Notably, Welsh’s team found that the CFTR protein is responsible for transporting chloride, allowing chloride ions to pass across the cell membrane. Next, Welsh’s team worked out the mechanisms through which that chloride channel functions — when the channel opens, when it closes, and what regulates that opening and closing. Finally, they described the major ways that mutations disrupt CFTR functioning and thus lead to cystic fibrosis, including the delta F508 mutation, which accounts for approximately 70 percent of all mutations causing cystic fibrosis and about 90 percent of all cystic fibrosis cases in the United States. 

He then asked if the delta F508 protein could be repaired. His group discovered that the mutation was temperature sensitive — when they lowered the temperature of cells, they were excited to find first, that the misprocessed delta F508 protein moved to its normal location on the cell surface, and second, that once there, it functioned as a chloride channel, although it did not open as well as the normal protein. These two discoveries, along with the others made by Welsh, paved the way for finding therapeutic medications. 

Negulescu, at Vertex Pharmaceuticals, then got to work to find remedies to treat the underlying cause of the disease. “Really where our work started was with the understanding that the most common mutation caused both a processing and functional defect. It set the stage for us to develop assays and to begin screening for compounds and developing medicines to restore and rescue the function of the defective protein,” says Negulescu. He says that one of the challenges of this work was that “there really was not a road map.” There had never been any pharmaceutical therapies before this that had done what he needed to do: Develop two types of medications. One medication — called a corrector — would restore the function of the protein so that it correctly finds its way to the surface of the cell. A second medication — called a potentiator — would enable the protein to function properly once it reached the cell’s surface. 

One product that Negulescu’s team came up with, known commercially as TRIKAFTA, contains three medications: two correctors and one potentiator. The treatment can help more than 90 percent of people living with cystic fibrosis. TRIKAFTA has helped increase the current life expectancy of patients as well. Today, according to the Cystic Fibrosis Foundation, for people with cystic fibrosis who were born between 2019 and 2023, the median age of survival is now predicted to be 61 years. 

Both Negulescu and Welsh credit the patients with cystic fibrosis and their families that they have interacted with over the course of their careers for continuing to inspire their research. “You can study it in textbooks, you can study the protein in the lab, but I felt I didn’t truly understand the disease until I spoke with people who had cystic fibrosis and their families, and they taught us a lot,” Negulescu says. He credits one patient for helping him steer his team toward a pill versus an inhaled medication. “I’ll never forget this conversation,” says Negulescu. “It was a young man probably in his 20s. He said, ‘Whatever you do, do not give us another inhaled therapy…my lungs have difficulty taking medications. Secondly, cystic fibrosis affects my entire body, not just my lung. So please, please do something to affect cystic fibrosis throughout my body.’” 

An appetizing spread that saves lives 

André Briend is the 2025 recipient of the John Dirks Canada Gairdner Global Health Award, which recognizes outstanding achievements in global health research. Briend received this award for his invention of a Ready-to-Use Therapeutic Food (RUTF) that has revolutionized how severe acute malnutrition is treated in children.

Back in the 1980s, Briend was doing research in Senegal and Bangladesh on how to treat children with severe malnutrition. At the time, the standard treatment was to admit children to the hospital where they would receive a mixture of water, skimmed milk powder, sugar, and oil, as well as other vitamins and mineral supplements. This formula had to be administered in the hospital because the liquid could accidentally become contaminated with bacteria. “All these constraints made the treatment of all malnourished children with a high risk of dying impossible,” says Briend.

He then set to work to develop a food that would be both highly nutritious and not contain water, which is what was most likely to lead to bacterial proliferation in case of accidental contamination. Working with Michel Lescanne, who just started the food company, Nutriset, which produced the formula given to malnourished children in the hospital — something called F-100 or “therapeutic milk” — he explored numerous options for foods that were nutritious, calorie-dense, high in fat, and shelf stable that didn’t require water. It was much harder than he thought, says Briend. “We explored many options, from doughnuts to high fat bars, pancakes and biscuits, but all of them had problems. Biscuits seemed the most convenient, but when the fat content was increased, they crumbled and were difficult to transport. Also, vitamins were damaged during the cooking process,” he says.

The team’s “aha moment” came when they realized that a popular chocolate spread had a proportion of fat, carbohydrate, and protein very similar to that of F-100. Further, they could use peanut butter to replace part of the dried skim milk. This new spread contained no water. It also did not grow bacteria when they experimentally contaminated a sample to see if bacteria would grow. Further, the spread is prepared without baking, which makes the inclusion of heat sensitive vitamins very easy, says Briend. “We also found that this fat and sweet spread had a very pleasant taste which masked the presence of the unpalatable mineral and vitamin mix present in WHO F-100.”

RUTF came with a bit of resistance as many people in Briend’s field didn’t think children or others who needed the RUTF would actually like a spread, and would prefer a liquid option. However, when they finally tested it, it became clear that some 80 percent of the children who would have otherwise needed to be hospitalized could be treated at home with this food product. “Now, severe acute malnutrition is seen as a condition amenable to mass treatment. Detection of high-risk children with mid-upper arm circumference (MUAC) is often carried out by families themselves and treatment with RUTF developed rapidly after the endorsement by WHO and UNICEF,” Briend says. 

Of receiving this reward, Briend says: “The best reward I get from my work is feedback I receive from many people treating children with severe acute malnutrition and telling me that they are transforming the lives of thousands of children.” 

Empowering kids and youth with pain through digital innovation

Jennifer Stinson is a 2025 recipient of the Peter Gilgan Canada Gairdner Momentum Award, which recognizes mid-career investigators for their exceptional scientific research contributions which continue to impact human health.

Stinson was awarded this honor for her international leadership in digital therapeutics focused on relieving pain in children with chronic conditions such as Juvenile Idiopathic Arthritis, Sickle Cell Disease, Chronic Pain, and Cancer as well as her international initiatives to train the next generation of child and youth pain researchers and clinicians.

Chronic pain, which impacts about 1 in 5 children and youth, is often under-recognized and under-treated. In fact, healthcare professionals receive less pain training than veterinarians, says Stinson. As a nurse practitioner, Stinson says she witnessed first-hand the devastating impact of illness-related chronic pain on the lives of children, youth, and their families. She is the first nurse clinician-scientist to receive a Canada Gairdner award.

After completing her PhD at the University of Toronto’s Lawrence Bloomberg Faculty of Nursing, Stinson set out to transform how chronic pain is understood and treated. She began by helping to develop the chronic pain program at The Hospital for Sick Children (SickKids), which is now the largest and most research-intensive pain clinic in Canada. 

She and her research group led a Canada-wide initiative that found most patients and their families want better access to treatments for young people with chronic pain. To bridge this gap, she employed the use of technology to help kids and teens better manage their pain. Her team created ‘iCanCope with Pain’, a smartphone-based app that has features such as daily check-ins and personal goal planning with tailored strategies to help with pain and other symptoms and social support. Her team also developed ‘iPeer2Peer’, a virtual peer mentoring program where young adults who have successfully moved on to adult care are matched with a teen with the same condition. This program is currently used by a national organization supporting youth with Juvenile Idiopathic Arthritis. During the pandemic, Stinson’s team created a one-stop online pain management resource called ‘Power over Pain Portal for Youth’ that provides free access to tools like iCanCope, in English and French. 

As technology continues to evolve, Stinson says she is committed to continuing to work on and improve the digital solutions her team developed. “It typically takes 17 years for an innovation to make its way from the research lab into clinical care. The current pace of change in technology makes it essential to find new ways of efficiently evaluating digital health interventions without compromising scientific rigour.” Stinson says that as a seasoned nurse practitioner, she is well positioned to directly translate new innovations into practice. “My lab is exploring the use of adaptive trial designs to meet this need, by more rapidly evaluating these technologies,” she says.

Stinson credits not only her peers and mentors over the years for helping to enable her success, but she credits her patients she has worked with in the Chronic Pain Clinic as well. One patient in particular, a 15-year-old girl living with chronic nerve pain following a minor sports injury, left a significant mark. “She was very determined to beat the pain,” Stinson says. “In fact, she went on to volunteer in my lab, was a mentor in the iPeer2Peer program, and then worked as coordinator in my lab while she completed her Masters of Science. She is now a PhD student in my lab working on the iCanCope app, adding a stigma support intervention for youth with sickle cell disease and helps co-lead our patient engagement work.” 

Tricking cancer cells to self-destruct 

Daniel De Carvalho is a 2025 recipient of the Peter Gilgan Canada Gairdner Momentum Award, recognizing mid-career investigators for their exceptional scientific research contributions which continue to impact human health.

De Carvalho was awarded this honor for his ground-breaking discovery of the role of transposable elements in regulating anti-tumor immunity through viral mimicry, which holds transformative potential for cancer therapy, and for pioneering the development of a novel blood-based test for early cancer detection, classification, and therapy monitoring.

De Carvalho received his PhD in cancer immunology, followed by postdoctoral training in cancer epigenetics. His lab currently focuses on the intersection of cancer epigenetics and cancer immunology. Epigenetic changes are “chemical modifications to the DNA without change to the DNA sequence itself,” De Carvalho says. “My research has been focused on the concept that, in cancer, you always have disruption in the epigenetic machinery.”

Over the past several years, De Carvalho has focused on what’s now called viral mimicry, a circumstance where, with the help of various treatments or therapies, a cancer cell is tricked into generating an immune response as if it were infected by a virus. ”We named this process viral mimicry because you mimic viral infection in the cancer cell” De Carvalho says. “The viral mimicry is a way to induce a very strong, optimal response against cancer cells.” This phenomenon could help boost the outcomes of other treatments such as immunotherapy and is currently being tested in clinical trials.

The other component of De Carvalho’s award is his team’s discovery and development of a novel blood test to detect cancer. After discovering that specific epigenetic changes, such as DNA methylation, in cancer cells can be detected in the blood, his team was able to create a test that detects these signatures. The first available test will be for head and neck cancer, but the mechanism through which this test works has the ability to potentially transform how cancer is detected and tracked.

In regards to receiving this award, De Carvalho says it has always been the work itself that brings him the greatest joy. “The science is the reward in itself,” says De Carvalho. “The clinical translation starting to help patients. That’s the biggest reward.”

About the Gairdner Foundation

The mission of the Gairdner Foundation is to celebrate, inform and inspire scientific excellence around the globe.

Established in 1957, the Gairdner Foundation is dedicated to fulfilling James A. Gairdner’s vision to recognize major research contributions to the treatment of disease and alleviation of human suffering. Through the prestigious annual Canada Gairdner Awards, the Foundation celebrates the world’s most creative and accomplished researchers whose work is improving the health and wellbeing of people around the world. Since its inception, 426 awards have been bestowed on laureates from over 40 countries, and of those awardees, 102 have gone on to receive Nobel Prizes.

The Gairdner Foundation brings people together to openly discuss science in order to better engage the public, understand the problems we face, and work together to find solutions. Through Gairdner Connects, our national outreach program, we bring science to communities across Canada to inspire future innovators and spark public dialogue about the role of research in addressing the world’s most pressing health challenges.