SAN DIEGO, CA – In 1977, when David R. Parkinson, MD, graduated from medical school at the University of Toronto and moved to McGill University to train in internal medicine and eventually hematology, the idea of medical oncology was in its infancy. In Canada, the profession didn’t exist.
“In Canada, there were no medical oncologists,” Parkinson told Inside Precision Medicine. “Radiation therapists administered what little chemotherapy existed. They resisted the development of medical oncology as a specialty.”
David R. Parkinson, MD, recipient of the 2026 AACR Outstanding Achievement Award for Service to Cancer Science and Medicine [The American Association for Cancer Research (AACR)]
Through the ensuing 49 years, Parkinson didn’t just see the rise of kinase inhibitors, antibodies, and cell therapies in real-time—he helped create the world of modern cancer therapeutics.
In reflecting on his remarkable career, which was recognized with the 2026 AACR Outstanding Achievement Award for Service to Cancer Science and Medicine, Parkinson said, “I’ve essentially grown alongside the field.”
From scarcity to structure: Oncology’s early years
When Parkinson arrived in Montreal, there were only a handful of chemotherapeutics available. “In those days, there were only one or two drugs available for hematologic malignancies across the entire field,” Parkinson said. “The main treatments were cyclophosphamide and nitrosoureas.”
Even supportive care lagged. “Initially, we had no effective way to control chemotherapy-induced nausea,” he noted of the standard of care for testicular cancer. “Some patients stopped treatment because they couldn’t tolerate it.”
Parkinson explained that early cancer drugs worked best on rapidly dividing tumors, like leukemias and testicular cancers, because that’s what the animal models represented. These therapies targeted DNA and cell division broadly, often with severe toxicity, and were far less effective against slower-growing solid tumors.
After his residency at McGill, Parkinson moved to Boston, first to Tufts New England Medical Center on a modest Canadian fellowship that placed him at the edge of a field just beginning to coalesce. “I was on a Canadian fellowship earning $12,000 a year,” he said. “The exchange rate fluctuated significantly, which made things difficult, and I couldn’t work due to my student visa.”
What he found, however, was momentum. Through connections with Dana-Farber, Parkinson entered formal training in medical oncology as the specialty began to take shape. “I connected with Dana-Farber and took their introductory course for fellows—that was my entry into medical oncology.”
At the same time, breakthroughs in specific cancers hinted at what might be possible. “What really shaped my thinking was the emergence of treatments for testicular cancer just as I entered oncology,” he said. “Platinum-based therapies—and later combination regimens—felt like miracles. We had never seen anything like it. These were often young patients, difficult to manage, but suddenly there were real cures.”
Targeted therapy and the Gleevec moment
Parkinson’s career soon intersected with early efforts to harness the immune system against cancer—decades before immunotherapy became a dominant paradigm. “I became deeply involved in immunotherapy, particularly interleukin-2 and early tumor-infiltrating lymphocyte studies,” he said.
Working at the National Cancer Institute (NCI), he collaborated with leaders, including immunotherapy pioneer Steven Rosenberg, MD, PhD, maintaining a hybrid role that combined research with clinical care. “At the same time, I continued clinical work for a couple of months each year, collaborating with Steve Rosenberg in the surgical branch.”
These early approaches were technically challenging and often unpredictable, but they laid the groundwork for later advances. “We started with basic approaches, moved to tumor-infiltrating lymphocytes, and eventually to engineered CAR T cells,” Parkinson said. “Progress has been steady, though often slower than those treating patients would like.”
If immunotherapy represented one trajectory, targeted therapy represented another—one that depended on a deeper understanding of cancer biology.
“When I joined Novartis in the late 1980s, we were among the first developing kinase inhibitors,” Parkinson said. At the time, the idea was controversial. “Early skepticism suggested kinase inhibitors wouldn’t work due to high intracellular ATP levels and structural challenges.”
But advances in molecular biology were beginning to change the landscape. The discovery of the Philadelphia chromosome and its associated oncogene created a clear therapeutic target. “The Philadelphia chromosome had been known since the 1960s, and by the 1980s the responsible gene was identified,” Parkinson explained.
The result was imatinib (Gleevec), a drug that would become a prototype for precision oncology. “Eventually, a small molecule inhibitor was developed that targeted it precisely.”
The clinical results were extraordinary. “By the third cohort in a Phase I trial, patients with chronic myelogenous leukemia showed dramatic responses—some within 24 hours,” Parkinson said. “It’s probably the only Phase I oncology trial where essentially every patient achieved remission.”
For Parkinson, the implications extended far beyond a single drug. “Of course, [Gleevec] was a unique case,” he said. “But it proved an important point: what once seemed impossible can become possible.”
Since then, the field has expanded dramatically. Hundreds of kinase inhibitors have been developed, with thousands more explored, reflecting a broader shift toward therapies grounded in specific molecular mechanisms.
Precision medicine—and its limits
As oncology evolved, so too did its language. “For years, we called it ‘personalized medicine,’” Parkinson said. “I used to joke that medicine has always been personalized—you’re always trying to determine what’s best for a specific patient in a specific context.”
He credits industry with popularizing a more precise term. “Although Pfizer popularized the term ‘precision medicine,’ I think it’s a better term,” he added, with a note of humor: “I have a few good Pfizer jokes—best shared over a drink.”
Yet the reality of precision medicine has proven more complex than its promise. “The evolution of therapeutics mirrored the models and biological understanding available,” Parkinson said. “Targeted therapies only emerged once we understood the biology. Diagnostics, however, lagged by about two decades.”
That lag remains a structural challenge. Parkinson founded a diagnostics company based on single-cell signaling technology developed at Stanford. “Technically, it worked—we solved major challenges in instrumentation, standardization, and analysis,” he said. “But we couldn’t establish a viable business model.”
The core issue was reimbursement. “Without adequate reimbursement from Medicare, even highly sophisticated diagnostics struggle commercially,” said Parkinson. “Better diagnostics can reduce the use of expensive drugs by identifying who won’t benefit—something that doesn’t always align with pharmaceutical business models.”
In recent years, Parkinson has focused increasingly on large-scale data integration, including his involvement with the GENIE consortium. The initiative aggregates genomic and clinical data across institutions, aiming to accelerate discovery and improve clinical decision-making. “GENIE has been a technical success,” he said. “But its long-term sustainability remains uncertain.”
The broader challenge, he argues, is conceptual as much as technical. “Looking forward, the field is evolving toward integrating multiple data types—genomics, transcriptomics, imaging, and more—to better understand tumor biology,” he said. “Sequencing alone isn’t enough. The challenge now is not a lack of data, but making sense of it—something where artificial intelligence will play an increasingly important role.”
Back to basics
Across academia, government, and industry—including roles at the NCI, Novartis, Amgen, and Biogen Idec—Parkinson sees a single throughline. “I remember an interview with a biotech company where an HR representative told me, ‘You seem to have done a lot of different things,’” he said. “I responded that I had really only done one thing: trying to improve cancer treatment, just from many different angles.”
Not every effort succeeded. “In one case, we developed a drug that performed beautifully in mice but failed in human trials,” he said. “That’s common in oncology—most ideas don’t translate. You don’t think of it as failure but as learning. Still, there’s a limit to how many ‘learnings’ one can appreciate.”
Reflecting on decades of progress, Parkinson emphasizes both how far the field has come and how much remains unresolved. “Outcomes have improved dramatically across several cancers, especially hematologic ones,” he said.
Yet he underscores a fundamental principle: that progress in cancer treatment comes down to understanding biology. “The better we understand it, the more effectively we can develop targeted therapies,” said Parkinson. “Without that understanding, we’re essentially guessing.”
At AACR 2026, Parkinson’s recognition underscores not just past achievements but a continuing trajectory—one shaped by the interplay of discovery, failure, and persistence. “Despite all the challenges,” he said, “[precision medicine] is still the most promising path forward.”
Get your daily dose of health and medicine every weekday with STAT’s free newsletter Morning Rounds. Sign up here.
Earth Day is next week, meaning it’s time for one of my favorite traditions: listening to the annual 24-hour livestream of a marsh in unceded W̱SÁNEĆ territory in British Columbia.
Approximately one in six adolescents and young adults who survive cancer will be diagnosed with another cancer within 30 years of their initial diagnosis, making their cancer risk more than double that of the general population, shows data from Canada.
“When combined with the relatively high survival rates in this age range, at approximately 86%, there is a growing population of young cancer survivors that will be adversely affected by their cancer diagnosis and its treatment even decades later,” write Miranda Fidler-Benaoudia, a cancer epidemiologist at the University of Calgary Cumming School of Medicine and Cancer Care Alberta, and co-authors in the Canadian Medical Association Journal.
“Given that subsequent primary neoplasms are major contributors to morbidity and premature mortality, these findings underscore the need for innovative solutions to prevent, detect, and treat subsequent primary neoplasms among survivors of adolescent and young adult cancer,” they say.
Although global data suggest that adolescent and young adult cancer survivors are 1.6 to 4.3 times more likely to develop a subsequent cancer than expected in the general population, data are limited for Canada, where cancer rates among this group increased annually by 1.3% from 1998 to 2012, with an estimated 8739 adolescents and young adults diagnosed with cancer in 2022.
The Alberta Adolescent and Young Adult Cancer Survivor Study retrospectively reviewed data for 24,459 people with a neoplasm first diagnosed between 1983 and 2017 at age 15 to 39 years. Of these, 1442 (5.9%) had subsequent primary neoplasms, 1129 (7.6%) of which occurred among the 14,818 people who were five-year survivors.
The researchers report that, overall, adolescent and young adult cancer survivors were 2.2 times more likely to develop a subsequent primary neoplasm than would be expected in the general population, equating to 31.7 excess neoplasms per 10,000 person–years.
For five-year survivors, the incidence was twofold higher versus the general population with an excess risk of 35.7 per 10,000 person–years.
The greatest excess risks occurred among survivors of breast cancer (85.8 per 10,000 person–years), lymphomas other than Hodgkin lymphoma or non-Hodgkin lymphoma (82.0 per 10,000 person–years), and oral cavity, lip, and pharyngeal cancer (74.7 per 10,000 person–years).
Conversely, no significant excesses were observed for survivors of acute myeloid leukemia, central nervous system cancers, ovarian cancer, nonovarian and nontesticular gonadal and related tumors, stomach cancer, lung, bronchial, and tracheal cancer, and endometrial cancer.
After five-year survival, the 30-year cumulative incidence of a subsequent primary neoplasm was 17.7% overall, with incidence highest among survivors of cancers of the oral cavity, lip, or pharynx (28.9%), breast cancer (27.3%), colon cancer (23.5%), and Hodgkin lymphoma (22.7%).
Importantly, the team found that the absolute difference in cumulative incidence between the survivors and general population grew as time since diagnosis increased; for example, for five-year survivors of breast cancer, the absolute difference was 2.9% at 10 years postdiagnosis compared with 12.7% at 30 years postdiagnosis.
“Although people with nearly all types of adolescent and young adult cancer investigated were at an increased risk of developing a subsequent primary neoplasm, survivors of Hodgkin lymphoma and breast cancer were identified as particularly vulnerable populations, with nearly one-third of subsequent primary neoplasms occurring after five-year survival diagnosed in these survivor groups,” Fidler-Benaoudia et al remark. “These findings are consistent with previous studies and reflect the established late effects of radiotherapy, chemotherapy, and hormone therapy.”
However, they also note that genetic factors may play a role, and that genetic counseling and education on maintaining healthy lifestyles are important in caring for survivors.
The most common subsequent primary neoplasms were breast (27.1%), digestive (11.9%), hematopoietic (10.6%), or respiratory (6.8%) cancers, together accounting for nearly 60% of subsequent primary neoplasms.
Fidler-Benaoudia and colleagues say that their findings “offer valuable directions for research and cancer control.”
They point out that at present there are no risk-based survivorship care guidelines that cover the entire age range of the adolescent and young adult cancer population.
“Although both pediatric and adolescent and young adult cancer survivors are at increased risks for late effects, the magnitude of these risks varies and implications for care can differ; thus, clinical investigations that assess the association of treatment exposures with late effects like subsequent primary neoplasms should be a research priority,” the authors write.
They also stress that further work is needed to expand inclusion criteria for early high-risk screening initiatives and to develop specialized treatment guidelines that balance curing the subsequent primary neoplasm while effectively managing the survivors’ late effects.
MIT Technology Review Explains: Let our writers untangle the complex, messy world of technology to help you understand what’s coming next. You can read more from the series here.
Just before Artemis II began its historic slingshot around the moon, Jared Isaacman, the recently confirmed NASA administrator, made a flurry of announcements from the agency’s headquarters in Washington, DC. He said the US would soon undertake far more regular moon missions and establish the foundations for a base at the lunar south pole before the end of the decade. He also affirmed the space agency’s commitment to putting a nuclear reactor on the lunar surface.
These goals were largely expected—but there was still one surprise. Isaacman also said NASA would build the first-ever nuclear reactor-powered interplanetary spacecraft and fly it to Mars by the end of 2028. It’s called the Space Reactor-1 Freedom, or SR-1 for short. “After decades of study, and billions spent on concepts that have never left Earth, America will finally get underway on nuclear power in space,” he said at the event. “We will launch the first-of-its-kind interplanetary mission.”
A successful mission would herald a new era in spaceflight, one in which traveling between Earth, the moon, and Mars would—according to a range of experts—be faster and easier than ever. And it might just give the US the edge in the race against China—allowing the country to beat its greatest geopolitical rival to landing astronauts on another planet.
While experts agree the timeline is extremely tight, they’re excited to see if America’s space agency and its industry partners can deliver an engineering miracle. “You wake up to that announcement, and it puts a big smile on your face,” says Simon Middleburgh, co-director of the Nuclear Futures Institute at Bangor University in Wales.
Little detail on SR-1 is publicly available, and NASA’s own spaceflight researchers did not respond to requests for comment. But MIT Technology Review spoke to several nuclear power and propulsion experts to find out how the new nuclear-powered spacecraft might work.
Nuclear propulsion 101
Traditionally, spaceflight has been powered by chemical propulsion. Liquefied hydrogen and liquefied oxygen are mixed, and then ignited, within a rocket; the searingly hot exhaust from this explosion is ejected through a nozzle, which propels the rocket forth.
Chemical propulsion offers a significant amount of thrust and will, for the foreseeable future, still be used to launch spacecraft from Earth. But nuclear propulsion would enable spacecraft to fly through the solar system for far longer, and faster, than is currently possible.
“You get more bang per kilogram,” says Middleburgh. A nuclear fuel source is far more energy-dense than its conventional cousin, which means it’s orders of magnitude more efficient. “It’s really, really, really high efficiency,” says Lindsey Holmes, an expert in space nuclear technology and the vice president of advanced projects at Analytical Mechanics Associates, an aerospace company in Virginia.
The approach also removes one other element of the traditional power equation: solar. Spacecraft, including the Artemis II mission’s Orion space capsule, often rely on the sun for power. But this can be a problem, since it doesn’t always shine in space, particularly when a planet or moon gets in its way—and as you head toward the outer solar system, beyond Mars, there’s just less sunlight available.
To circumvent this issue, nuclear energy sources have been used in spacecraft plenty of times before—including on both Voyager missions and the Saturn-interrogating Cassini probe. Known as radioisotope thermoelectric generators, or RTGs, these use plutonium, which radioactively decays and generates heat in the process. That heat is then converted into electricity for the spacecraft to use. RTGs, however, aren’t the same as nuclear reactors; they are more akin to radioactive batteries—more rudimentary and considerably less powerful.
So how will a nuclear-reactor-powered spacecraft work?
Despite operational differences, the fundamentals of running a nuclear reactor in space are much the same as they are on Earth. First, get some uranium fuel; then bombard it with neutrons. This ruptures the uranium’s unstable atomic nuclei, which expel a torrent of extra neutrons—and that rapidly escalates into a self-sustaining, roasting-hot nuclear fission reaction. Its prodigious heat output can then be used to produce electricity.
Doing this in space may sound like an act of lunacy, but it’s not: The idea, and even a lot of the basic technology, has been around for decades. The Soviet Union sent dozens of nuclear reactors into orbit (often to power spy satellites), while the US deployed just one, known as SNAP-10A, back in 1965—a technological demonstration to see if it would operate normally in space. The aim was for the reactor to generate electricity for at least a year, but it ran for just over a month before a high-voltage failure in the spacecraft caused it to malfunction and shut down.
Now, more than half a century later, the US wants its second-ever space-based nuclear reactor to do something totally different: power an interplanetary spacecraft.
To be clear, the US has started, and terminated, myriad programs looking into nuclear propulsion. The latest casualty was DRACO, a collaboration between NASA and the Department of Defense, which ended in 2025. Like several previous efforts, DRACO was canceled because of a mix of high experimentation costs, lower prices for conventional rocket propulsion, and the difficulty of ensuring that ground tests could be performed safely and effectively (they are creating an incredibly powerful nuclear reaction, after all).
But now external considerations may be changing the calculus. The Artemis program has jump-started America’s return to the moon, and the new space race has palpable momentum behind it. The first nation to deploy nuclear propulsion would have a serious advantage navigating through deep space.
“I think it’s a very doable technology,” says Philip Metzger, a spaceflight engineering researcher at the Florida Space Institute.“I’m happy to see them finally doing this.”
One version of this technology is known as nuclear thermal propulsion, or NTP. You start with a nuclear reactor, one that’s cooking at around 5,000°F. Then “you’ve got a cold gas, and you squirt cold gas over the hot reactor,” says Middleburgh. “The gas expands, you shoot it out the back of a nozzle, and you have an impulse. And that impulse drives you forward.”
Because the thrust depends on the speed of the gas being ejected, the propellant gas needs to be light, making hydrogen a popular choice. But hydrogen is a corrosive and explosive substance, so using it in NTP engines can make them precarious to operate. On top of this, NTP doesn’t necessarily have a very long operating life.
Alternatively, there’s nuclear electric propulsion, or NEP, which “is very low thrust, but very efficient, so you can use it for a long period of time,” says Sebastian Corbisiero, the US Department of Energy’s national technical director of space reactor programs. This method uses heat from a fission reactor to generate power. That power is used to electrify a gas and then blast it out of the spacecraft, generating thrust.
Both NTP and NEP have been investigated by US researchers, because both have the added benefit of making it easier and safer for human beings to explore the solar system. Astronauts in space are exposed to harmful cosmic radiation, but because nuclear propulsion makes spacecraft speedier and more agile, they’d spend less time in it. “It solves the radiation problem,” says Metzger. “That’s one of the main motivations for inventing better propulsion to and from Mars.”
How to build a nuclear-powered spaceship
For SR-1, NASA has opted for nuclear electric propulsion. NEP is “a much simpler affair” than its thermal counterpart, says Middleburgh. Essentially, you just need to plug a nuclear reactor into a power-and-propulsion system. Luckily for NASA, it’s already got one.
For many years, NASA—along with its space agency partners in Canada, Europe, Japan, and the Middle East—was preparing for Gateway, meant to be humanity’s first space station to orbit around the moon. Isaacman canceled the project in March, but that doesn’t mean its technology will go to waste; the power-and-propulsion element of the nixed space station will be used in SR-1 instead. This contraption was going to be powered by solar energy. It’ll now be attached to an in-development nuclear reactor custom built to survive in space.
What might the SR-1 look like? MIT Technology Review saw a presentation by Steve Sinacore, program executive of NASA’s Space Reactor Office, that offers some clues. So far, the concept art makes it look like a colossal fletched arrow. At the back will be the power-and-propulsion system, while its tip will hold a 20-kilowatt-or-greater uranium-filled nuclear reactor. (For context, a typical nuclear plant on Earth is 50,000 times more powerful, producing a gigawatt of power.)
NASA
The “fletches” on SR-1 are large fins that allow the reactor to cool down. “You have to have really large radiators,” says Holmes, since the nuclear fission process produces so much heat that much of it has to be vented into space—otherwise, the reactor and spacecraft will melt.
According to that presentation, the spacecraft’s hardware development is due to start this June. By January 2028, SR-1’s systems should be ready for assembly and testing. And by that October, the spacecraft will arrive at the launch site, ready for liftoff before the year’s end. Will the nuclear reactor manage to hold itself together? “Going through the launch safely is going to be a challenge,” says Middleburgh. “You are being shaken, rattled, and rolled.”
Then, he says, “once you’re up in space, once you’ve got through that few minutes of hell in getting there, it’s zero-gravity considerations you have to worry about.” The question then becomes: Will the mechanics of the reactor, built on terra firma, still work?
For safety reasons, the nuclear reactor will be switched on around two days post-launch, when it’s comfortably in space. Uranium isn’t tremendously dangerous by itself, but that can’t be said of the nuclear waste products that emerge when the reactor is activated, so you don’t want any of that to fall back to Earth.
If this schedule is adhered to, and SR-1 works as planned, it’s expected to reach Mars about a year after launch. “It’s an aggressive timeline,” says Holmes, something she suspects is being driven partly by China’s and Russia’s own deep-space nuclear ambitions. The two countries aim to place their own nuclear reactor on the moon’s surface to power the planned International Lunar Research Station—a jointly operated lunar base—by 2035.
Whether it flies or fails in space, SR-1’s operations should help NASA with putting a nuclear reactor on the moon soon after. “All of the things we’d be learning about how that system operates in space [are] very helpful for a surface application, because basically it’s the same,” says Corbisiero. “There’s still no air on the moon.”
And if SR-1 does triumph, it will be a game-changing victory for NASA. It will also be “a massive win for the human race, frankly,” says Middleburgh. “It will be a marvel of engineering, and it will move the dial in humans potentially taking a step on Mars.” Like many of his colleagues, including Holmes, he remains thrilled by the prospect of the first-ever nuclear-powered interplanetary spacecraft—even with the incredibly ambitious timeline.
“These are the things that get us up in the morning,” he says. “These are the sorts of things we will remember when we’re old.”
Studying mice, researchers at Toronto’s Sinai Health have found that semaglutide—the active ingredient in popular weight loss drugs that mimic the gut hormone GLP-1—acts directly on a subset of liver cells to improve organ function, and does so independently of weight loss. The finding challenges long-held assumptions about how GLP-1 medicines work in the liver and could reshape how physicians treat metabolic liver disease.
For years, the liver benefits of semaglutide have puzzled scientists. “Glucagon-like peptide-1 (GLP-1) medicines improve metabolic liver disease through weight-loss-dependent and -independent actions,” the authors wrote. The drug was known to lower blood sugar and promote weight loss, but patients’ livers were improving in ways that those effects alone could not explain. And as the authors further noted, “The therapeutic scope of GLP-1 medicines extends beyond glycemic control and weight loss, with benefits evident in people with atherosclerotic heart disease, heart failure with preserved ejection fraction (HFpEF), peripheral artery disease, diabetic kidney disease, knee osteoarthritis, and obstructive sleep apnea (OSA).” However, as the team further pointed out, “… the mechanisms by which GLP-1 medicines improve organ dysfunction remain incompletely understood.”
Drucker has been at the forefront of GLP-1 research since the 1980s when his pioneering discoveries helped lay the groundwork for the development of GLP-1 medicines. After transforming treatment of type 2 diabetes and obesity, semaglutide and other GLP-1 medicines have been approved for other conditions including MASH (metabolic dysfunction-associated steatohepatitis). MASH is a severe form of fatty liver disease in which fat build-up, inflammation, and tissue scarring can lead to cirrhosis and liver failure. It affects about 25% Canadian adults and because it is closely linked with obesity and type 2 diabetes, treatment typically includes lifestyle interventions to reduce weight. “The approval of semaglutide for MASH highlights the importance of understanding the hepatoprotective mechanisms of GLP-1 action,” the investigators stated.
Drucker and colleagues have now found that semaglutide acts directly on the liver to reduce inflammation and scarring and improve organ function in a way that is independent of weight loss. Their finding overturns a prevailing assumption in the field that liver cells do not carry the receptor that semaglutide binds to, meaning the drug had no direct route to the organ.
Postdoctoral researcher Maria Gonzalez-Rellan, PhD, spearheaded the work that combined sophisticated mouse models of MASH with deep molecular analyses of liver cells. Her work identified two cell types carrying semaglutide receptors: liver sinusoidal endothelial cells (LSECs) and immune T cells. Although LSECs account for only about 3% of liver cell volume, they proved to be the key driver of semaglutide’s liver benefits.
A pioneer in GLP-1 biology, Daniel Drucker, MD, has dedicated his career to understanding how the GLP-1 hormone, and the therapies derived from it, function in the body. His early discovery that GLP-1 stimulates insulin secretion in a glucose-dependent manner paved the way for today’s widely popular medications for type 2 diabetes and obesity. Drucker’s ongoing research continues to shine light on the less understood aspects of GLP-1 biology including its effects on the liver and in regulating inflammation. [Colin Dewar, Sinai Health]
LSECs line the tiniest blood vessels in the liver and are studded with pores that allow them to act as a molecular sieve, filtering substances passing between the liver and the bloodstream. Gonzalez-Rellan showed that semaglutide reversed MASH in mice that lacked the brain receptors controlling appetite, demonstrating that weight loss is not required for liver benefits. “Unexpectedly. semaglutide improves hepatic inflammation, fibrosis, and immune remodeling through actions on Glp1r+ pericentral liver sinusoidal ECs (LSECs) independent of changes in body weight (BW),” the team reported. “… we leveraged a unique model of GLP-1R deficiency, Glp1rWnt1-/- mice, which are resistant to GLP-1RA-induced weight loss. Remarkably, semaglutide markedly improved hepatic steatosis, fibrosis, and immune remodeling in the absence of weight reduction.”
In a further test, mice lacking LSEC receptors showed no liver improvement on semaglutide even after losing 20% of their body weight. Detailed molecular analyses of liver cell types showed that semaglutide shifts gene activity in LSCEs, prompting them to release anti-inflammatory molecules that act on the broader liver environment, pushing it toward a state more closely resembling a healthy, disease-free liver. “Together, the data using mouse models of MASH reveal an EC-specific, weight-loss-independent, semaglutide-regulated, GLP-1R-dependent intrahepatic network for improving liver health,” the scientists said.
“It turns out that the receptor responsible for these benefits is in a very specialized population of liver cells,” commented Drucker, who is also a professor of medicine at the University of Toronto. “And this receptor orchestrates the production of molecules that talk to many different types of liver cells to calm down the inflammatory environment that is the problem in metabolic disease.”
The findings carry practical implications. GLP-1 medicines have become widely prescribed, yet their mechanism of action in the body, beyond appetite suppression and blood sugar control, have remained incompletely understood. Knowing that semaglutide improves liver health independently of weight loss could influence prescribing decisions. “We’ve seen in clinical trials that patients who lose very little weight see the same reductions in liver inflammation, scarring and enzyme levels as those who lose a great deal of weight. Now we know why,” Drucker pointed out. In their paper the team concluded “Hence, semaglutide produces a broad proteomic remodeling of the liver, enabling restoration of metabolic homeostasis and suppression of fibrogenic and inflammatory programs. The strong concordance between single-cell transcriptional changes, bulk tissue proteomics, and biomarker signatures underscores the breadth of GLP-1R-mediated hepatic reprogramming.”
Physicians may choose lower doses that avoid the side effects associated with the higher doses needed for significant weight loss, potentially also lowering costs for patients, Drucker suggested adding “We’re not saying weight loss isn’t important because many things improve when patients lose weight. But we now know that weight shouldn’t be the only measure of success, because GLP-1 medicines will improve liver health whether or not the patient loses weight.”
The American Association for Cancer Research (AACR) has released the names of the recipients of several annual professional awards. These awards recognize outstanding accomplishments and achievements in cancer research, therapy development, education, mentorship, and more. The honorees, listed below, will give lectures during this year’s meeting, which is being held in San Diego, CA. This year’s meeting runs from April 17-22.
AACR Lifetime Achievement in Cancer Research Award
James P. Allison, PhD, FAACR
This award honors individuals who have made fundamental contributions to cancer research through a single scientific discovery or a body of work. Allison is being recognized for his contributions to cancer research and patient care. Most notably, he is being celebrated for his identification of CTLA-4 as a negative regulator of T-cell activation, an insight that has since been translated into a first-in-class therapy that revitalized the field of cancer immunology and led to a revolution in cancer immunotherapies. Allison is a fellow of the AACR Academy, a professor and chair of the department of immunology, vice president for immunobiology, and the founding director of the James P. Allison Institute at the University of Texas MD Anderson Cancer Center.
AACR Outstanding Achievement in Basic Cancer Research Award
Housheng Hansen He, PhD
This award recognizes early-career investigators for meritorious achievements in basic cancer research. He is a professor in the department of medical biophysics at the University of Toronto and a senior scientist in the Princess Margaret Cancer Center. He is recognized for contributions to cancer epigenetics and RNA medicine, particularly in revealing how chromatin accessibility and epigenomic landscapes govern oncogenic transcription. His studies of FOXA1-androgen receptor networks, noncoding RNAs, and RNA modifications have improved scientists’ understanding of tumor progression, plasticity, and therapeutic resistance.
AACR Outstanding Achievement in Blood Cancer Research Award
John F. DiPersio, MD, PhD
This award recognizes individuals with meritorious achievements and contributions to blood cancer research.DiPersio is this year’s recipient for his work in leukemia and stem cell biology, including essential contributions to the development of the hematopoietic stem cell mobilizing agents plerixafor and motixafortide. DiPersio identified AK1/2 signaling in graft-versus-host disease, which led to the identification and approval of JAK inhibitors, including ruxolitinib (Jakafi). DiPersio is the Virginia E. and Sam J. Golman professor of medicine and a professor of medicine, immunology, and pathology at Washington University School of Medicine in St. Louis. He is also director of the Center for Gene and Cellular Immunotherapy at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine.
AACR Outstanding Achievement in Chemistry in Cancer Research Award
Cheryl H. Arrowsmith, PhD
This award honors individuals who have done novel and significant chemistry research that has led to important contributions in basic and translational cancer research, cancer diagnosis, prevention, and treatment. Arrowsmith is being recognized for foundational studies defining the structure and function of chromatin-associated proteins that regulate gene expression in cancer. Her work enabled the development of chemical probes that target epigenetic regulators. She is a senior scientist at the Princess Margaret Cancer Centre, University Health Network and chief scientist of the Structural Genomics Consortium. She is also a professor in the department of medical biophysics at the University of Toronto.
AACR Daniel D. Von Hoff Award for Outstanding Contributions to Education and Training in Cancer Research
Charles W.M. Roberts, MD, PhD, FAACR
This award recognizes significant contributions to education and training for cancer scientists and physicians at any career level. Roberts is a fellow of the AACR Academy and the executive vice president and director of the St. Jude Comprehensive Cancer Center. He is also a member in the department of oncology and the Lillian R. Cannon Comprehensive Cancer Center Director Endowed Chair at the St. Jude Children’s Research Hospital. This award recognizes his leadership and dedication to the education and training of cancer researchers across the spectrum of childhood cancer research, including basic, translational, clinical, and population science.
AACR James S. Ewing-Thelma B. Dunn Award for Outstanding Achievement in Pathology in Cancer Research
David L. Rimm, MD, PhD
The award celebrates pathologists who have contributed to advancing cancer research, diagnosis, treatment, and prevention. Rimm is recognized this year for innovations in quantitative biomarker science that transformed cancer diagnostics and treatment. His invention of the fluorescence-based Automated Quantitative Analysis platform improved immunohistochemistry by enabling precise, reproducible protein quantification in tissue specimens. Rimm is the Anthony N. Brady professor of pathology, a professor of medicine in oncology, director of quantitative diagnostics in the anatomic pathology lab, director of Yale Pathology Tissues Services, and director of the physician scientist training program in pathology at Yale University School of Medicine. He is also a member of Yale Cancer Center and director of the Yale Cancer Center Tissue Microarray Facility.
AACR Margaret Foti Award for Leadership and Extraordinary Achievements in Cancer Research
Antoni Ribas, MD, PhD, FAACR
This award recognizes individuals whose leadership and achievements contributed to the acceleration of progress against cancer, raising national or international awareness of the importance of cancer research, among other achievements. Ribas is being recognized for contributions to melanoma biology and cancer immunotherapy that were instrumental to the clinical development of pembrolizumab (Keytruda) and other transformative therapies. His research helped define mechanisms of immunotherapy response and resistance, which guided the design of innovative combination therapy approaches. Ribas is a fellow of the AACR Academy and AACR Past President. He is also a professor of medicine, surgery, and molecular and medical pharmacology at the University of California Los Angeles (UCLA), as well as director of the tumor immunology program at the UCLA Jonsson Comprehensive Cancer Center. He also serves as the director of the Parker Institute for Cancer Immunotherapy Center at UCLA.
AACR Team Science Award
The Cancer Dependency Map (DepMap) team
This award recognizes interdisciplinary research teams for science that advances or is likely to advance our fundamental knowledge of cancer, or a team that has applied existing knowledge to advance the detection, diagnosis, prevention, or treatment of cancer. The Broad Institute Cancer Dependency Map (DepMap) team is recognized this year for systematically mapping genetic dependencies across cancer cells and creating a comprehensive resource that reveals genes and pathways essential for tumor survival. By combining large-scale CRISPR functional genomic screens, drug response data, and multiomic profiling, the team uncovered lineage- and genotype-specific cancer vulnerabilities, including synthetic lethal dependencies such as WRN in microsatellite instability cancers and PRMT5 dependencies in cancers with MTAP deletions.
AACR American Cancer Society Award for Research Excellence in Cancer Epidemiology and Prevention
Elizabeth A. Platz, ScD, MPH
This award recognizes research accomplishments in cancer epidemiology, biomarkers, and prevention. Platz is the Martin D. Abeloff, MD Scholar in Cancer Prevention in the epidemiology department at the Johns Hopkins Bloomberg School of Public Health. She is also the associate director of population sciences at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. This award recognizes her contributions to scientists’ understanding of prostate cancer development, progression, and prevention. Her research linked intraprostatic inflammation to prostate cancer risk, identified telomere length patterns as prognostic biomarkers, and demonstrated protective associations between statin use, cholesterol, and disease lethality.
AACR Cancer Research Institute Lloyd J. Old Award in Cancer Immunology
Kenneth M. Murphy, MD, PhD
This award recognizes scientists whose research has had a major impact on the cancer field and has the potential to stimulate new directions in cancer immunology. Murphy is the Eugene Opie First Centennial Professor in pathology and immunology at the Washington University School of Medicine in St. Louis. This award recognizes his work on discoveries related to the development and functional specialization of dendritic cell subsets that regulate adaptive immune responses. His work elucidated the transcriptional programs that control dendritic cell lineage commitment, including the role of transcription factors such as BATF3 in the development of cross-presenting dendritic cells required to prime cytotoxic T-cell responses.
AACR G.H.A. Clowes Award for Outstanding Basic Cancer Research
Andrew P. Feinberg, MD, MPH
This award, which has the distinction of being AACR’s oldest award, recognizes individuals who have made outstanding recent accomplishments in basic cancer research. Feinberg is recognized this year for discoveries about the fundamental role of epigenetic alterations in cancer, including the identification of early, widespread DNA methylation abnormalities and the role of genomic imprinting in tumor development. His research demonstrated that large-scale epigenomic alterations contribute to tumor initiation, progression, and cellular heterogeneity, leading to the concept of epigenetic plasticity as a driver of cancer evolution. Feinberg is the Bloomberg Distinguished Professor at the Johns Hopkins University Schools of Medicine, Engineering, and Public Health. He also serves as director of the Center for Epigenetics of the Institute for Basic Biomedical Sciences.
AACR Irving Weinstein Foundation Distinguished Lectureship Award
Dennis Lo, DM, DPhil
The recipient for this award is selected by the AACR president, and acknowledges individuals whose personal innovation in science and whose position as a thought leader in fields relevant to cancer research have the potential to inspire creative thinking and new directions in cancer research. Lo is the vice-chancellor and president of the Chinese University of Hong Kong, where he also serves as the Li Ka Shing Professor of Medicine and professor of chemical pathology. He is being recognized for his discovery of fetal DNA in maternal plasma. Lo was the first to identify cell-free fetal DNA and fetal epigenetic markers in maternal plasma, enabling safer and earlier prenatal diagnostics. He also demonstrated that DNA released by tumors may be used for cancer screening, an insight that led to the development of circulating DNA-based tools for early cancer detection and screening.
AACR Joseph H. Burchenal Award for Outstanding Achievement in Clinical Cancer Research
Luis A. Diaz Jr., MD, FAACR
This award recognizes outstanding achievements in clinical cancer research. Diaz, a fellow of the AACR Academy, heads the division of solid tumor oncology and is the Grayer Family Chair at the Memorial Sloan Kettering Cancer Center. This award recognizes his pioneering discoveries such as biomarker-driven immunotherapies and for demonstrating that tumors with mismatch repair deficiencies and microsatellite instability are highly responsive to immune checkpoint blockade. Diaz has also advanced the use of circulating tumor DNA to detect minimal residual disease and led clinical trials of PD-1 blockade in mismatch repair-deficient cancers.
AACR Minorities in Cancer Research Jane Cooke Wright Lectureship
Ahmedin M. Jemal, DVM, PhD
This lectureship recognizes scientists with meritorious contributions to the field of cancer research and who have furthered the advancement of minority investigators in cancer research. This year’s awardee is recognized for research that quantified temporal and geographic trends in cancer burden using large-scale analysis of cancer registries, mortality rates, and risk factor data, and identified population-level determinants of cancer incidence, survival, and stage at diagnosis across demographic groups. Jemal’s work linked changes in risk factor exposure, screening uptake, and treatment advances to declines in cancer mortality and informed strategies for cancer prevention, early detection, and population-level cancer control. He is the senior vice president of the Surveillance, Prevention, & Health Services Research department at the American Cancer Society. He is also an adjunct professor in the department of epidemiology at the Rollins School of Public Health at Emory University.
AACR Princess Takamatsu Memorial Lectureship
David C. Lyden, MD, PhD
This award recognizes individual scientists whose work has had or may have a far-reaching impact on the detection, diagnosis, treatment, or prevention of cancer. Lyden is the Stavros S. Niarchos Professor in pediatric cardiology and professor of pediatrics at Weill Cornell Medicine. He is also director of the physician-scientist training program in pediatrics, a founding member of the Drukier Institute for Children’s Health and a member of the Sandra and Edward Meyer Cancer Center. He is being recognized for describing how primary tumors systemically promote metastasis by forming pre-metastatic niches in distant organs. Lyden’s research demonstrated that tumor-derived extracellular vesicles and exomeres, together with bone marrow-derived progenitor cells, remodel distant microenvironments and determine organ-specific metastatic tropism.
AACR St. Baldrick’s Foundation Award for Outstanding Achievement in Pediatric Cancer Research
Kimberly Stegmaier, MD, FAACR
This award recognizes individuals who have contributed to pediatric cancer research, resulting in the fundamental improvement of the understanding and/or treatment of pediatric cancer. Stegmaier serves as chair in the department of pediatric oncology at Dana-Farber Cancer Institute and the David G. Nathan professor of pediatrics at Harvard Medical School. She is also the associate chief of the division of hematology/oncology at Boston Children’s Hospital and an institute member at the Broad Institute. This award recognizes her genomic discoveries that defined the molecular landscape of childhood cancers and led to the identification of key drivers of fusion oncoprotein positive malignancies. Her research used systematic functional genomic screening and chemical biology strategies to identify critical dependencies in high-risk acute leukemias and pediatric solid tumors.
AACR Waun Ki Hong Award for Outstanding Achievement in Translational and Clinical Cancer Research
Eliezer M. Van Allen, MD
This award recognizes cancer researchers under the age of 51 who have conducted meritorious translational and clinical cancer research anywhere in the world. Van Allen is the Chandra Nohria Family Chair for AI in Cancer Research and chief of the division of population sciences at Dana-Farber Cancer Institute. He is also a professor of medicine at Harvard Medical School and an institute member at the Broad Institute. Through large-scale tumor sequencing and integrative genomic analyses, Van Allen’s research defined genomic mechanisms underlying resistance to targeted therapies, including BRAF inhibition in melanoma, and identified genomic features associated with response to immune checkpoint blockade. His work has advanced biomarker discovery and the use of genomic data to guide personalized cancer treatments, as well as bridged advances in artificial intelligence with translational cancer research.
AACR Women in Cancer Research Charlotte Friend Lectureship
Maryellen L. Giger, PhD
This award recognizes scientists’ contributions to the cancer research field and those who have furthered the advancement of women in science through leadership or by example. Giger is the A.N. Pritzker Distinguished Service Professor of Radiology at the University of Chicago. Giger’s research has established quantitative imaging and radiomics approaches that extract high-dimensional features from radiologic images to characterize tumor phenotype and predict cancer risk, diagnosis, and treatment response. She has also guided more than 120 trainees and consistently championed the careers of women scientists and clinicians.
Pezcoller Foundation-AACR International Award for Extraordinary Achievement in Cancer Research
Douglas R. Lowy, MD, FAACR and John T. Schiller, PhD, FAACR
This award is presented to international scientists who have made a scientific discovery in basic cancer research or who have made significant contributions to translational cancer research. Lowy is principal deputy director of the National Cancer Institute (NCI) and chief of the Laboratory of Cellular Oncology at NCI. Schiller is deputy chief of the Laboratory of Cellular Oncology at NCI and chief of the lab’s neoplastic disease section. Both awardees are also fellows of the AACR Academy and NIH Distinguished Investigators. They are being recognized for pioneering the molecular and immunologic foundations of human papillomavirus vaccines, engineering virus-like particles for safe and effective immunization, and driving their translation into global cancer prevention strategies that have dramatically reduced cervical and other HPV-related cancer incidence.
<![CDATA[“Each person the right to tell their own story in their own way”: An Italian-Canadian psychiatrist traces family journeys across 3 countries, revealing migration’s lessons on identity, belonging, and resilience.]]>
Is it the Department of Defense or the Department of War? The Gulf of Mexico or the Gulf of America? A vaccine—or an “individualized neoantigen treatment”?
That’s the Trump-era vocabulary paradox facing Moderna, the covid-19 shot maker whose plans for next-generation mRNA vaccines against flus and emerging pathogens have been dashed by vaccine skeptics in the federal government. Canceled contracts and unfriendly regulators have pushed the Massachusetts-based biotech firm to a breaking point. Last year, Robert F. Kennedy Jr., head of the Department of Health and Human Services, zeroed in on mRNA, unwinding support for dozens of projects—including a $776 million award to Moderna for a bird flu vaccine. By January, the company was warning it might have to stop late-stage programs to develop vaccines against infections altogether.
That raises the stakes for a second area of Moderna’s research. In a partnership with Merck, it’s been using its mRNA technology to destroy tumors through a very, very promising technique known as a cancer vacc—
“It’s not a vaccine,” a spokesperson for Merck jumped in before the V-word could leave my mouth. “It’s an individualized neoantigen therapy.”
Oh, but it is a vaccine. And here’s how it works. Moderna sequences a patient’s cancer cells to find the ugliest, most peculiar molecules on their surface. Then it packages the genetic code for those same molecules, called neoantigens, into a shot. The patient’s immune system has its orders: Kill any cells with those yucky surface markers.
Mechanistically, it’s similar to the covid-19 vaccines. What’s different, of course, is that the patient is being immunized against a cancer, not a virus.
And it looks like a possible breakthrough. This year, Moderna and Merck showed that such shots halved the chance that patients with the deadliest form of skin cancer would die from a recurrence after surgery.
In its formal communications, like regulatory filings, Moderna hasn’t called the shot a cancer vaccine since 2023. That’s when it partnered up with Merck and rebranded the tech as individualized neoantigen therapy, or INT. Moderna’s CEO said at the time that the renaming was to “better describe the goal of the program.” (BioNTech, the European vaccine maker that’s also working in cancer, has shifted its language too, moving from “neoantigen vaccine” in 2021 to “mRNA cancer immunotherapies” in its latest report.)
The logic of casting it as a therapy is that patients already have cancer—so it’s a treatment as opposed to a preventive measure. But it’s no secret what the other goal is: to distance important innovation from vaccine fearmongering, which has been inflamed by high-ranking US officials. “Vaccines are maybe a dirty word nowadays, but we still believe in the science and harnessing our immune system to not only fight infections, but hopefully to also fight … cancers,” Kyle Holen, head of Moderna’s cancer program, said last summer during BIO 2025, a big biotech event in Boston.
Not everyone is happy with the word games. Take Ryan Sullivan, a physician at Massachusetts General Hospital who has enrolled patients in Moderna’s trials. He says the change raises questions over whether trial volunteers are being properly informed. “There is some concern that there will be patients who decline to treat their cancer because it is a vaccine,” Sullivan told me. “But I also felt it was important, as many of my colleagues did, that you have to call it what it is.”
But is it worth going to the mat for a word? Lillian Siu, a medical oncologist at the Princess Margaret Cancer Centre, in Toronto, who has played a role in safety testing for the new shots, watches US politics from a distance. She believes name change is acceptable “if it allows the research to continue.”
Holen told me the doctors complaining to Moderna were basically motivated by a desire to defend vaccines—which are, of course, among the greatest public health interventions of all time. They wanted the company to stand strong.
But that’s not what’s happening. When Moderna’s latest results were published in February, the paper’s main text didn’t use the word “vaccine” at all. It was only in the footnotes that you could see the term—in the titles of old papers and patents.
All this could be a sign that Kennedy’s strategy is working. His agencies often appear to make mRNA vaccines a focus of people’s worries, impede their reach, devalue them for companies, and sideline their defenders.
Still, Moderna’s strategy may be working too. So far, at least, the government hasn’t had much to say about the company’s cancer vacc— I mean, its individualized neoantigen therapy.
This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.
The Mental Health Commission of Canada is pleased to welcome Shauna Cronin (she/her) as our new Vice President, Programs, effective April 27, 2026.
Shauna brings nearly two decades of national leadership in mental health system transformation, program design, and policy innovation. Her experience spans complex, multi‑partner initiatives across governments, communities, and lived and living experience networks, with notable contributions through organizations such as CAMH, Frayme, Stepped Care Solutions 2.0, and the Global Leadership Exchange.
A widely respected and internationally recognized leader, Shauna is known for turning bold vision into measurable impact. Her work has consistently advanced equity, strengthened service integration, and elevated Canada’s leadership in mental health, while meaningfully valuing First Nations, Inuit, and Métis voices as part of an ongoing reconciliation journey.
Shauna holds advanced degrees in political science, strategic communications, and international affairs, is currently pursuing a Master’s in Nonprofit and Philanthropic Leadership, and holds a Health Leadership designation from the Rotman School of Management. She brings a rare combination of deep policy insight, collaborative systems leadership, and a genuine commitment to people and outcomes.
We look forward to the perspective, care, and leadership Shauna will bring as she joins our exceptional Programs team and helps advance mental health and well-being across Canada.
A rare warm spell in January melted enough snow to uncover Cornell University’s newest athletic field, built for field hockey. Months before, it was a meadow teeming with birds and bugs; now it’s more than an acre of synthetic turf roughly the color of the felt on a pool table, almost digital in its saturation. The day I walked up the hill from a nearby creek to take a look, the metal fence around the field was locked, but someone had left a hallway-size piece of the new simulated grass outside the perimeter. It was bristly and tough, but springy and squeaky under my booted feet. I could imagine running around on it, but it would definitely take some getting used to.
My companion on this walk seemed even less favorably disposed to the thought. Yayoi Koizumi, a local environmental advocate, has been fighting synthetic-turf projects at Cornell since 2023. A petite woman dressed that day in a faded plum coat over a teal vest, with a scarf the colors of salmon, slate, and sunflowers, Koizumi compulsively picked up plastic trash as we walked: a red Solo cup, a polyethylene Dunkin’ container, a five-foot vinyl panel. She couldn’t bear to leave this stuff behind to fragment into microplastic bits—as she believes the new field will. “They’ve covered the living ground in plastic,” she said. “It’s really maddening.”
The new pitch is one part of a $70 million plan to build more recreational space at the university. As of this spring, Cornell plans to install something like a quarter million square feet of synthetic grass—what people have colloquially called “astroturf” since the middle of the last century. University PR says it will be an important part of a “health-promoting campus” that is “supportive of holistic individual, social, and ecological well-being.” Koizumi runs an anti-plastic environmental group called Zero Waste Ithaca, which says that’s mostly nonsense.
This fight is more than just the usual town-versus-gown tension. Synthetic turf used to be the stuff of professional sports arenas and maybe a suburban yard or two; today communities across the United States are debating whether to lay it down on playgrounds, parks, and dog runs. Proponents say it’s cheaper and hardier than grass, requiring less water, fertilizer, and maintenance—and that it offers a uniform surface for more hours and more days of the year than grass fields, a competitive advantage for athletes and schools hoping for a more robust athletic program.
But while new generations of synthetic turf look and feel better than that mid-century stuff, it’s still just plastic. Some evidence suggests it sheds bits that endanger users and the environment, and that it contains PFAS “forever chemicals”—per- and polyfluoroalkyl substances, which are linked to a host of health issues. The padding within the plastic grass is usually made from shredded tires, which might also pose health risks. And plastic fields need to be replaced about once a decade, creating lots of waste.
Yet people are buying a lot of the stuff. In 2001, Americans installed just over 7 million square meters of synthetic turf, just shy of 11,000 metric tons. By 2024, that number was 79 million square meters—enough to carpet all of Manhattan and then some, almost 120,000 metric tons. Synthetic turf covers 20,000 athletic fields and tens of thousands of parks, playgrounds, and backyards. And the US is just 20% of the global market.
Where real estate is limited and demand for athletic facilities is high, artificial turf is tempting. “It all comes down to land and demand.”
Frank Rossi, professor of turf science, Cornell
Those increases worry folks who study microplastics and environmental pollution. Any actual risk is hard to parse; the plastic-making industry insists that synthetic fields are safe if properly installed, but lots of researchers think that isn’t so. “They’re very expensive, they contain toxic chemicals, and they put kids at unnecessary risk,” says Philip Landrigan, a Boston College epidemiologist who has studied environmental toxins like lead and microplastics.
But at Cornell, where real estate is limited and demand for athletic facilities is high, synthetic turf was a tempting option. As Frank Rossi, a professor of turf science at Cornell, told me: “It all comes down to land and demand.”
In 1965, Houston’s new, domed baseball stadium was an icon of space-age design. But the Astrodome had a problem: the sun. Deep in the heart of Texas, it shined brightly through the Astrodome’s skylights—so much so that players kept missing fly balls. So the club painted over the skylights. Denied sunlight, the grass in the outfield withered and died.
A replacement was already in the works. In the late 1950s a Ford Foundation–funded educational laboratory determined that a soft, grasslike surface material would give city kids more places to play outside and had prevailed upon the Monsanto corporation to invent one. The result was clipped blades of nylon stuck to a rubber base, which the company called ChemGrass. Down it went into Houston’s outfield, where it got a new, buzzier name: AstroTurf.
Workers lay artificial turf at the Astrodome in Houston on July 13, 1966. Developed by Monsanto, the material was originally known as ChemGrass but was later renamed AstroTurf after the stadium.
AP PHOTO/ED KOLENOVSKY, FILE
That first generation of simulated lawn was brittle and hard, but quality has improved. Today, there are a few competing products, but they’re all made by extruding a petroleum-based polymer—that’s plastic—through tiny holes and then stitching or fusing the resulting fibers to a carpetlike bottom. That gets attached to some kind of padding, also plastic. In the 1970s the industry started layering that over infill, usually sand; by the 1990s, “third generation” synthetic turf had switched to softer fibers made of polyethylene. Beneath that, they added infill that combined sand and a soft, cheap shredded rubber made from discarded automobile tires, which pile up by the hundreds of millions every year. This “crumb rubber” provides padding and fills spaces between the blades and the backing.
In the early 1980s, nearly half the professional baseball and football fields in the US had synthetic turf. But many players didn’t like it. It got hotter than real grass, gave the ball different action, and seemed to be increasing the rate of injuries among athletes. Since the 1990s, most pro sports have shifted back toward grass—water and maintenance costs pale in comparison to the importance of keeping players happy or sparing them the risk of injury.
But at the same time, more universities and high schools are buying the artificial stuff. The advantages are clear, especially in places where it rains either too much or not enough. A natural-grass field is usable for a little more than 800 hours a year at the most, spread across just eight months in the cooler, wetter northern US. An artificial-turf field can see 3,000 hours of activity per year. For sports like lacrosse, which begins in late winter, this makes artificial turf more appealing. Most lacrosse pitches are now synthetic. So are almost all field hockey pitches; players like the way the even, springy turf makes the ball bounce.
Furthermore, supporters say synthetic turf needs less maintenance than grass, saving money and resources. That’s not always true; workers still have to decompact the playing surface and hose it off to remove bird poop or cool it down. Sometimes the infill needs topping up. But real grass allows less playing time, and because grass athletic fields often need to be rotated to avoid damage, synthetic ground cover can require less space. Hence the market’s explosive growth in the 21st century.
The city and town of Ithaca—two separate political entities with overlapping jurisdiction over Cornell construction projects—held multiple public meetings about the university’s new synthetic fields: the field hockey pitch and a complex called the Meinig Fieldhouse. Koizumi’s group turned up in force, and a few folks who worked at Cornell came to oppose the idea too—submitting pages of citations and studies on the risks of synthetic grass.
At two of those meetings, dozens of Cornell athletes turned out to support the turf. Representatives of the university and the athletic department declined to speak with me for this story, citing an ongoing lawsuit from Zero Waste Ithaca. But before that, Nicki Moore, Cornell’s director of athletics, told a local newspaper that demand from campus groups and sports teams meant the fields were constantly overcrowded. “Activities get bumped later and later, and sometimes varsity teams won’t start practicing until 10 at night, you know?” Moore told the paper. “Availability of all-weather space should normalize scheduling a great deal.”
That argument wasn’t universally convincing. “It’s a bad idea, but that’s from the environmental perspective,” says Marianne Krasny, director of Cornell’s Civic Ecology Lab and one of the speakers at those hearings. “Obviously the athletic department thinks it’s a great idea.”
GETTY IMAGES
Members of Cornell on Fire, a climate action group with members from both the university and the town, joined in opposing the use of artificial turf, citing the fossil-fuel origins of the stuff. They described the nominal support of the project from student athletes as inauthentic, representing not grassroots support but, yes, an astroturf campaign.
Sorting out the actual science here isn’t simple. Over time, the plastic that synthetic turf is made of sheds bits of itself into the environment. In one study, published in 2023 in the journal Environmental Pollution, researchers found that 15% of the medium-size and microplastic particles in a river and the Mediterranean Sea outside Barcelona, Spain, came from artificial turf, mostly in the form of tiny green fibers. Back in 2020, the European Chemicals Agency estimated that infill material from artificial-turf fields in the European Union was contributing 16,000 metric tons of microplastics to the environment each year—38% of all annual microplastic pollution. Most of that came from the crumb rubber infill, which Europe now plans to ban by 2031.
This pollution worries the Cornell activists. Ithaca is famous for scenic gorges and waterways. The new field hockey pitch is uphill from a local creek that empties into Cayuga Lake, the longest of the Finger Lakes and the source of drinking water for over 40,000 people.
And it’s not just the plastic bits. When newer generations of synthetic turf switched to durable high-density polyethylene, the new material gunked up the extruders used in the manufacturing process. So turf makers started adding fluorinated polymers—a type of PFAS. Some of these environmentally persistent “forever chemicals” cause cancer, disrupt the endocrine system, or lead to other health problems. Research in several different labs has found PFAS in many types of plastic grass.
But the key to assessing the threat here is exposure. Heather Whitehead, an analytical chemist then at the University of Notre Dame, found PFAS in synthetic turf at levels around five parts per billion—but estimated it’d be in water running off the fields at three parts per trillion; for context, the US Environmental Protection Agency’s legal drinking-water limit on one of the most widespread and dangerous PFAS chemicals is four parts per trillion. “These chemicals will wash off in small amounts for long periods of time,” says Graham Peaslee, Whitehead’s advisor and an emeritus nuclear physicist who studies PFAS concentrations. “I think it’s reason enough not to have artificial turf.”
This gets confusing, though. There are over 16,000 different types of PFAS, few have been well studied, and different companies use different manufacturing techniques. Companies represented by the Synthetic Turf Council now “use zero intentionally added PFAS,” says Melanie Taylor, the group’s president. “This means that as the field rolls off the assembly line, there are zero PFAS-formulated materials present.”
Some researchers are skeptical of the industry’s assurances. They’re hard to confirm, especially because there are a lot of ways to test for PFAS. The type of synthetic turf going onto the new field hockey pitch at Cornell is called GreenFields TX; the university had a sample tested using an EPA method that looks for 40 different PFAS compounds. It came back negative for all of them. The local activists countered that the test doesn’t detect the specific types they’re most concerned about, and in 2025 they paid for three more tests on newly purchased synthetic turf. Two clearly found fluorine—the F in “PFAS”—and one identified two distinct PFAS compounds. (The company that makes GreenFields TX, TenCate, declined to comment, citing ongoing litigation.)
PFAS isn’t the only potential problem. There’s also the crumb rubber made from tires. A billion tires get thrown out every year worldwide, and if they aren’t recycled they sit in giant piles that make great habitats for rats and mosquitoes; they also occasionally catch fire. Lots of the tires that go into turf are made of styrene-butadiene rubber, or SBR. In bulk, that’s bad. Butadiene is a carcinogen that causes leukemia, and fumes from styrene can cause nervous system damage. SBR also contains high levels of lead.
But how much of that comes out of synthetic-turf infill? Again, that’s hotly debated. Researchers around the world have published suggestive studies finding potentially dangerous levels of heavy metals like zinc and lead in synthetic turf, with possible health risks to people using the fields. But a review of many of the relevant studies on turf and crumb rubber from Canada’s National Collaborating Centre for Environmental Health determined that most well-conducted health risk assessments over the last decade found exposures below levels of concern for cancer and certain other diseases. A 2017 report by the European Chemicals Agency—the same people who found all those microplastics in the environment—“found no reason to advise people against playing sports on synthetic turf containing recycled rubber granules as infill material.” And a multiyear study from the EPA, published in 2024, found much the same thing—although the researchers said that levels of certain synthetic chemicals were elevated inside places that used indoor artificial turf. They also stressed that the paper was not a risk assessment.
The problem is, the kinds of cancers these chemicals can cause may take decades to show up. Long-term studies haven’t been done yet. All the evidence available so far is anecdotal—like a series for the Philadelphia Inquirer that linked the deaths of six former Phillies players from a rare type of brain cancer called glioblastoma to years spent playing on PFAS-containing artificial turf. That’d be about three times the usual rate of glioblastoma among adult men, but the report comes with a lot of cautions—small sample size, lots of other potential causes, no way to establish causation.
Synthetic turf has one negative that no one really disputes: It gets very hot in the sun—as hot as 150 °F (66 °C). This can actually burn players, so they often want to avoid using a field on very hot days.
A field hockey player from Cornell University passes the ball during a game played on artificial turf at Bryant University in 2025. Cornell’s own turf field will be ready for the 2026 season.
GETTY IMAGES
Athletes playing on artificial turf also have a higher rate of foot and ankle injuries, and elite-level football players seem to be more predisposed to knee injuries on those surfaces. But other studies have found rates of knee and hip injury to be roughly comparable on artificial and natural turf—a point the landscape architect working on the Cornell project made in the information packet the university sent to the city. Athletic departments and city parks departments say that the material’s upsides make it worthwhile, given that there’s no conclusive proof of harm.
Back in Ithaca, Cornell hired an environmental consulting firm called Haley & Aldrich to assess the evidence. The company concluded that none of the university’s proposed installations of artificial turf would have a negative environmental impact. People from Cornell on Fire and Zero Waste Ithaca told me they didn’t trust the firm’s findings; representatives from Haley & Aldrich declined to comment.
Longtime activists say that as global consumption of fossil fuels declines, petrochemical companies are desperate to find other markets. That means plastics. “There’s a big push to shift more petrochemicals into plastic products for an end market,” says Jeff Gearhart, a consumer product researcher at the Ecology Center. “Industry people, with a vested interest in petrochemicals, are looking to expand and build out alternative markets for this stuff.”
All that and more went before the decision-makers in Ithaca. In September 2024, the City of Ithaca Planning Board unanimously issued a judgment that the Meinig Fieldhouse would not have a significant environmental impact and thus would not need to complete a full environmental impact assessment. Six months later, the town made the same determination for the field hockey pitch.
Zero Waste Ithaca sued in New York’s supreme court, which ruled against the group. Koizumi and lawyers from Pace University’s Environmental Litigation Clinic have appealed. She says she’s still hopeful the court might agree that Ithaca authorities made a mistake by not requiring an environmental impact statement from the college. “We have the science on our side,” she says.
Ithaca is a pretty rarefied place, an Ivy League university town. But these same tensions—potential long-term environmental and public health consequences versus the financial and maintenance concerns of the now—are pitting worried citizens against their representatives and city agencies around the country.
New York City has 286 municipal synthetic-turf fields, with more under construction. In Inwood, the northernmost neighborhood in Manhattan, two fields were approved via Zoom meetings during the pandemic, and Massimo Strino, a local artist who makes kaleidoscopes, says he found out only when he saw signs announcing the work on one of his daily walks in Inwood Hill Park, along the Hudson River. He joined a campaign against the plan, gathering more than 4,300 signatures. “I was canvassing every weekend,” Strino says. “You can count on one hand, literally, the number of people who said they were in favor.”
But that doesn’t include the group that pushed for one of those fields in the first place: Uptown Soccer, which offers free and low-cost lessons and games to 1,000 kids a year, mostly from underserved immigrant families. “It was turning an unused community space into a usable space,” says David Sykes, the group’s executive director. “That trumped the sort of abstract concerns about the environmental impacts. I’m not an expert in artificial turf, but the parks department assured me that there was no risk of health effects.”
Artificial turf doesn’t go away. “You’re going to be paying to get rid of it. Somebody will have to take it to a dump, where it will sit for a thousand years.”
Graham Peaslee, emeritus nuclear physicist studying PFAS concentrations, University of Notre Dame
New York City councilmember Christopher Marte disagrees. He has introduced a bill to ban new artificial turf from being installed in parks, and he hopes the proposal will be taken up by the Parks Committee this spring. Last session, the bill had 10 cosponsors—that’s a lot. Marte says he expects resistance from lobbyists, but there’s precedent. The city of Boston banned artificial turf in 2022.
Upstate, in a Rochester suburb called Brighton, the school district included synthetic-turf baseball and softball diamonds in a wide-ranging February 2024 capital improvement proposition. The measure passed. In a public meeting in November 2025, the school board acknowledged the intent to use synthetic grass—or, as concerned parents had it, “to rip up a quarter million square feet of this open space and replace it with artificial turf,” says David Masur, executive director of the environmental group PennEnvironment, whose kids attend school in Brighton. Parents and community members mobilized against the plan, further angered when contractors also cut down a beloved 200-year-old tree. School superintendent Kevin McGowan says it’s too late to change course. Masur has been working to oppose the plan nevertheless—he says school boards are making consequential decisions about turf without sharing information or getting input, even though these fields can cost millions of dollars of taxpayer money.
In short, the fights can get tense. On Martha’s Vineyard, in Massachusetts, a meeting about plans to install an artificial field at a local high school had to be ended early amid verbal abuse. A staffer for the local board of health who voiced concern about PFAS in the turf quit the board after discovering bullet casings in her tote bag, she said, which she perceived as a death threat. After an eight-year fight, the board eventually banned artificial turf altogether.
What happens next? Well, outdoor artificial turf lasts only eight to 12 years before it needs to be taken up and replaced. The Synthetic Turf Council says it’s at least partially recyclable and cites a company called BestPLUS Plastic Lumber as a purveyor of products made from recycled turf. The company says one of its products, a liner called GreenBoard that artificial turf can be nailed into, is at least 40% recycled from fake grass. Joseph Sadlier, vice president and general manager of plastics recycling at BestPLUS, says the company recycles over 10 million pounds annually.
Yet the material is piling up. In 2021, a Danish company called Re-Match announced plans to open a recycling plant in Pennsylvania and began amassing thousands of tons of used plastic turf in three locations. The company filed for bankruptcy in 2025.
In Ithaca, university representatives told planning boards that it would be possible to recycle the old artificial turf they ripped out to make way for the Meinig Fieldhouse. That didn’t happen. An anonymous local activist tracked the old rolls to a hauling company a half-hour’s drive south of campus and shared pictures of them sitting on the lot, where they stayed for months. It’s unclear what their ultimate fate will be.
That’s the real problem: Artificial turf just doesn’t go away. “You’re going to be paying to get rid of it,” says Peaslee, the PFAS expert. “Somebody will have to take it to a dump, where it will sit for a thousand years.” At minimum, real grass is a net carbon sink, even including installation and maintenance. Synthetic turf releases greenhouse gases. One life-cycle analysis of a 2.2-acre synthetic field in Toronto determined that it would emit 55 metric tons of carbon dioxide over a decade. Plastic fields need less water to maintain, but it takes water to make plastic, and natural grass lets rainwater seep into the ground. Synthetic turf sends most of it away as runoff.
It’s a boggling set of issues to factor into a decision. Rossi, the Cornell turf scientist, says he can understand why a school in the northern United States might go plastic, even when it cares about its students’ health. “It was the best bad option,” he says. Concerns about microplastics and PFAS are “significant issues we have not fully addressed.” And they need to be.
Douglas Main is a journalist and former senior editor and writer at National Geographic.
![A pioneer in GLP-1 biology Dr. Daniel Drucker has dedicated his career to understanding how the GLP-1 hormone, and the therapies derived from it, function in the body. His early discovery that GLP-1 stimulates insulin secretion in a glucose-dependent manner paved the way for today's widely popular medications for type 2 diabetes and obesity. Dr. Drucker's ongoing research continues to shine light on the less understood aspects of GLP-1 biology including its effects on the liver and in regulating inflammation. [Colin Dewar, Sinai Health]](https://www.genengnews.com/wp-content/uploads/2026/04/Low-Res_Drucker_LTRI_Colin_Dewar-225x300.jpeg)
