DALLAS – July 23, 2026 – Scientists have long sought to understand why some people with no known risk factors develop cancer while others with significant risk never do. The answer may lie in immune proteins known as autoantibodies (auto-Abs), suggests a commentary in Cell co-authored by a team that includes Jean-Laurent Casanova, M.D., Ph.D., Professor in the Center for the Genetics of Host Defense and Children’s Medical Center Research Institute at UT Southwestern (CRI).

Dr. Casanova, who has dual appointments in Pediatrics and Immunology, joined UT Southwestern Medical Center from The Rockefeller University on July 1 and brought his entire lab with him, including more than 40 scientists, trainees, and students. The Casanova Lab is part of the ATLAS team – short for Antibody Tracking for Long-term Avoidance and Surveillance – one of five research groups that received a Cancer Grand Challenges grant of up to $25 million earlier this year. Together, the team will investigate the potential role of auto-Abs in promoting and preventing cancer.

“There is ample evidence that the immune system plays a significant role in cancer,” Dr. Casanova said. “Our job will be to determine if there are auto-Abs that could offer protection against cancer or drive cancer outcomes, knowledge that could have a profound impact on cancer risk assessment and treatment.”

Jean-Laurent Casanova, M.D., Ph.D., is Professor in the Center for the Genetics of Host Defense and Children’s Medical Center Research Institute at UT Southwestern. He also has dual appointments in Pediatrics and Immunology.

Humans have billions of different antibodies, proteins randomly produced by the immune system that can bind to molecules known as antigens, including those found on bacteria, viruses, fungi, toxins, or allergens. Antibodies can neutralize these threats or mark them for destruction by immune cells, helping the body fight off infections. However, in people with autoimmune diseases, antibodies mistakenly bind to normal molecules in the body. These auto-Abs cause the immune system to attack healthy cells and tissues.

Research led by Dr. Casanova and others has shown that auto-Abs can target molecules called cytokines that the immune system uses to fight infectious diseases. He and other scientists have discovered auto-Abs that bind to about a dozen of the 50 or so known cytokines so far, with ongoing research in the Casanova Lab and elsewhere aiming to identify more. These auto-Abs have been linked to a growing range of infectious diseases, sometimes in significant proportions of patients, and even, more recently, to an inflammatory condition. As scientists have learned various ways the immune system interacts with cancer – findings that have resulted in immunotherapies such as checkpoint inhibitor drugs and chimeric antigen receptor (CAR) T-cells – a growing hypothesis has suggested that other auto-Abs could influence cancer development and growth.

To test this idea, the ATLAS team – led by Paul Bastard, M.D., Ph.D., in the Laboratory of Human Genetics of Infectious Diseases at Imagine Institute of the Necker Hospital for Sick Children in Paris – will catalog and study auto-Abs in a large and diverse group of volunteers. They will include people with genetic syndromes or behaviors known to promote cancer, such as heavy smokers, who have avoided the disease; aging individuals, including centenarians; identical and fraternal twins; and patients with cancers before, during, and after they receive immunotherapies. By better understanding the role of auto-Abs in cancer, Dr. Casanova explained, researchers can develop new ways to help patients reduce their cancer risk or treat existing disease more effectively.

This work is an extension of the Casanova Lab’s longstanding focus on inborn errors of immunity, genetic disorders that affect immune system function. Over three decades, Dr. Casanova and his colleagues have uncovered more than 80 genes that, when mutated, impair the body’s ability to fight off specific infections such as influenza, West Nile virus, and COVID-19. These inborn errors of immunity to infection led his lab to discover auto-Abs against cytokines, as their consequences mimic inborn errors of immunity. The lab will continue this research alongside the ATLAS project.

Dr. Casanova earned his medical degree at Paris Descartes University and went on to specialize in pediatrics. He completed his doctoral degree in immunology at the Pierre and Marie Curie University in Paris and co-founded the Laboratory of Human Genetics of Infectious Diseases at the Necker Hospital for Sick Children in Paris. He is a member of the National Academy of Sciences and the National Academy of Medicine and an Investigator of the Howard Hughes Medical Institute. His work has been recognized recently with two prestigious international awards: the 2026 Mechthild Esser Nemmers Prize in Medical Science and the 2025 Novo Nordisk Prize.

This year, he received a $5 million Governor’s University Research Initiative (GURI) grant as part of a program to recruit distinguished researchers to Texas colleges and universities.

ATLAS is funded by the Breast Cancer Research Foundation, Cancer Research UK, the Susan Wojcicki Foundation, and the Torrey Coast Foundation through Cancer Grand Challenges.

Dr. Casanova holds the Marilyn R. Corrigan Distinguished Chair in Pediatric Research. Dr. He holds the S. Roger and Carolyn P. Horchow Chair in Cardiac Research, in Honor of Jere H. Mitchell, M.D. Dr. Pomper holds the Effie and Wofford Cain Distinguished Chair in Diagnostic Imaging and is a member of the Chemistry, Biomedical Engineering, and Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 22, 2026 – Matteo Ligorio’s phone started buzzing just after 3 a.m. The texts from a hospice nurse indicated “Patient 14” had just passed away, which meant Dr. Ligorio and his team had less than four hours to honor her dying wish.

He pulled on his navy blue scrubs, climbed into his SUV, and sped through the mostly empty streets of Dallas to a clinic space operated by UT Southwestern Medical Center’s Willed Body Program. That’s where he would spend the next few hours performing a rapid autopsy designed to help answer one of the most enigmatic questions in modern medicine:

Why do people die from cancer?

Dr. Ligorio, a surgeon and researcher at UT Southwestern, believes he and his team have found the answer – and it’s probably not what you or most medical experts think.

“Macrovascular infiltration,” the phenomenon that occurs when cancer invades major blood vessels and unleashes clusters of circulating tumor cells (CTCs), marks the final physiological event before death from cancer, according to a one-of-a-kind study led and supervised by Dr. Ligorio and published in Nature Medicine. The CTCs form blood clots, triggering multiorgan failure, and that is the primary reason patients “die on one specific day rather than six months earlier or later,” he said.

Dr. Ligorio led the team during rapid autopsy procedures.

The findings challenge the widely accepted explanation that metastasis – the spread of cancer throughout the body to other organs – is the ultimate cause of most cancer-related deaths. In fact, when Dr. Ligorio first shared his theory with Kelley Newcomer, M.D., a palliative care specialist at UT Southwestern and the eventual lead author on the study, she politely told him: “It sounds fascinating … but I’m really worried you are wrong.”  

That was not the first time he’d heard that response.

But Dr. Newcomer agreed to take a deeper look. Together they retrospectively analyzed 108 autopsies from patients in Dallas who died of colorectal, lung, ovarian, liver, or pancreatic cancer, and she was amazed at what they found – macrovascular infiltration was detected on scans in 60% of the cases.

“You can see the storm coming,” Dr. Ligorio said.

He began developing this alternate theory of cancer progression about 20 years ago when he was a surgical resident at the University of Genoa in Italy. In 2011, he embarked on his “American Dream” at Harvard University, where he earned his Ph.D. in molecular epidemiology and biostatistics and started working closely with Nicola Aceto, Ph.D., who joined him as senior author on the Nature Medicine study, analyzing the role of CTCs in cancer mortality.

In 2020, Dr. Ligorio was recruited to investigate cancer biology at UT Southwestern, where he is an Assistant Professor of Surgery and a member of the Harold C. Simmons Comprehensive Cancer Center.

Six years later, he seems acutely aware that he’s standing on the precipice of a breakthrough.

“This is a theory. Like gravity. It still has to be proven,” he said, pointing to a phase 2/3 clinical trial he and his team are planning that will target macrovascular infiltration across tumor types. “But if we are right, and I believe we are, this discovery won’t just change the way we diagnose and treat cancer; it can change our ‘cultural’ perceptions of the disease.

“As long as we can prevent macrovascular infiltration – and we can do that with existing therapies – you can live with it. Cancer will not be the enemy it is now.”

Starting at the end

As a boy growing up in Italy, “Matte” loved solving mazes. He’d start at the end, tracing each route until he eventually worked his way out of the labyrinth.

Nowadays, when he’s describing his theory of macrovascular infiltration in one of the many presentations he’s given since the publication of the study in October 2025, he’ll often scribble a maze on a whiteboard and explain his core belief: The only way to truly know how and why cancer kills people is to start at the end of life.

Macrovascular infiltration, which the team suggests marks Stage V of cancer progression, can often be seen on a routine CT scan.

Enter Dr. Newcomer, an Associate Professor of Internal Medicine at UT Southwestern who specializes in hospice and palliative care. She and Dr. Ligorio met during the COVID-19 pandemic. Even while chatting over coffee, standing about 12 feet apart outdoors, she was impressed by his passion and bold ideas.

“Dr. Ligorio is a force of nature. It doesn’t take long to notice,” she said. “He can be very convincing.”

Together, they make an unlikely but complementary pair.

He’s a surgeon who grew up in Italy; she’s an internist born and raised in Dallas. His focus is on bench science; hers is at the bedside. He has a long list of international contacts and enjoys being the maestro of Zoom meetings with oncologists, pathologists, and data scientists from all over the world; she is embedded in the local community, counseling patients, families, and caregivers in their most intimate and difficult moments.

As Medical Director of Adult and Pediatric Hospice for the Visiting Nurse Association of Texas, Dr. Newcomer knew that many of the nurses, chaplains, and patients in hospice would embrace the chance to participate in important research.

Hospice patients like Peggy Moore, pictured with her husband of 40 years, Wayne, generously agreed to participate in the study to advance cancer discovery and future treatments.

“It might sound crazy, but basic science and hospice are a great pairing,” she said. “As scientists, you’re able to see very advanced disease states that have been previously unstudied. And most of these patients are excluded from clinical trials. But because they’ve decided to stop treatment and aren’t going back and forth to doctors’ appointments, they have extra time on their hands.

“Many of them also are examining their legacy and feel a strong urge to do something good for the world,” she added. “I think the study really helped them find meaning in a very devastating illness.”

Wayne Moore confirms as much. Peggy, his wife of 40 years and the love of his life, was “all in” when she heard about the research. 

“Peggy wasn’t one to dwell on her pancreatic cancer, or her life being shorter than either of us had expected,” he said. “She had spent much of her life looking out for others, and I think she saw this program – and playing even a small part in this important research – as a natural extension of that. To her, it was just the right thing to do, and I think it’s a fitting commentary on her legacy.”

Connecting the dots

Previously published research has shown that cancer, in its most advanced stages, can alter the cardiovascular system. The work by Dr. Ligorio, Dr. Newcomer, and their team, however, is the first to “provide compelling insights into circulatory alterations in patients approaching death,” according to a News & Views article in Nature Medicine highlighting the significance of their findings.

In one regard, their theory of cancer progression sounds like common sense. Cancer in organs located close to major vessels, such as the pancreas or lungs, is more lethal because tumors and cancer cells don’t have far to travel to invade the bloodstream. For cancers not located near major vessels, such as the prostate, thyroid, and breast, survival rates are much higher.

But proving causation and connecting the dots between three biological events – cancer invading major vessels, CTCs forming a clot and restricting blood flow, and death from multiorgan failure – is a much more complex and arduous process. For their study, Drs. Ligorio and Newcomer took the following steps:

• First, they performed the retrospective analysis of 108 routine clinical autopsies from William P. Clements Jr. University Hospital and Parkland Memorial Hospital between 2010 and 2020. About 60% of the usable scans showed signs of macrovascular infiltration.  
• Next, Dr. Newcomer recruited 31 hospice patients for the rapid autopsy study: 21 with solid tumors and 10 with other conditions to serve as the control group. Over the following weeks, she and her clinical team, which included Kathryn Naumann, Assistant Director of Clinical Research, and research nurse Sarah Reeves, monitored and examined the patients, taking blood samples whenever they reported a significant change in health status or when their score worsened on an assessment called the Palliative Performance Scale.
• When the patients died – an average of 38 days after they were enrolled – Dr. Ligorio performed a modified autopsy on each, sealing major blood vessels from the neck to the pelvis to preserve their integrity. About 40% of the patients with cancer had tumors penetrating the walls and extending into the interiors of major blood vessels. Dr. Ligorio captured 240 hours of video of the autopsies to show the scientific rigor with which they were conducted.
• To help validate the autopsy findings, Dr. Ligorio enlisted collaborators at the University of Lubeck and the University of Mainz in Germany to examine CT imaging data from 1,250 cancer patients. He also reached out to Dario Ghersi, M.D., Ph.D., Associate Professor at the University of Nebraska at Omaha and a former medical school colleague from Italy, to analyze the data along with computational scientist Kirk Gasper, Ph.D. Macrovascular infiltration prior to death was independently confirmed on many of the routine scans.

The team also worked closely with Dr. Aceto, now a Professor of Molecular Oncology at ETH Zurich in Switzerland, to analyze the blood samples from the hospice patients while they were still alive. Dr. Aceto has created a circulating tumor cell lab and used a device that can filter out CTCs in clusters from the blood. His analysis revealed a sharp uptick in cancer cells in the bloodstream just before death.

Dr. Newcomer recalls one case that captured the predictive power of their research.

She and the nursing team were visiting a patient who had developed jaundice almost overnight. The team arrived before dawn to draw blood, which was then express-shipped to Dr. Aceto’s lab in Zurich. Two days later he provided an ominous report: “This patient has considerable surge in circulating tumor cells, and it is hard to believe that this condition would be compatible with life.”

Dr. Newcomer thought, “No way. That is not what we saw. She seemed fine. In fact, she had woken up early to apply her makeup and make coffee for us.”

Less than 24 hours later, she died.

“You could see the end was near,” Dr. Newcomer said. “For me, that was a real ‘aha’ moment.”

Matteo Ligorio, M.D., Ph.D.

“As long as we can prevent macrovascular infiltration – and we can do that with existing therapies – you can live with it. Cancer will not be the enemy it is now.”

Kelley Newcomer, M.D.

“I think we are moving toward a scenario where cancer could become more of a chronic disease.”

 

 

Setting the stage for Stage 5

On a Thursday morning in Dallas, faces began filling up the Zoom screen for a meeting titled “The Stage 5 Consortium.”

Dr. Ligorio welcomed everyone in his lyrically accented English and started sharing updates. Preliminary results were strongly reinforcing the broader research premise that macrovascular infiltration is the fifth and final stage of cancer progression.

For more than 60 years, the internationally recognized standard for cancer progress – the Tumor Node Metastasis (TNM) System – has classified Stage 4 as the most advanced form of the disease. It’s characterized by the spread of cancer cells beyond the original site to other organs in the body. Even suggesting that there is a “Stage 5” is an audacious notion.

But Dr. Ligorio and his team are not shrinking from this prospect.

“For the first time in history, we have a theory that is testable, and I think that has created a lot of enthusiasm,” he said. It has also built momentum and some high-profile collaborations.

Robert Timmerman, M.D., is Chair and Professor of Radiation Oncology at UT Southwestern. He holds the Effie Marie Cain Distinguished Chair in Cancer Therapy Research.

Robert Timmerman, M.D., Chair and Professor of Radiation Oncology at UT Southwestern and a pioneer in stereotactic body radiation therapy (SBRT), will play a key role in shaping the upcoming clinical trial, which will employ precision radiation treatments and existing surgical techniques to target lesions near large blood vessels. A multicenter trial could also utilize implantable devices to deliver chemotherapy directly to tumors – one of Dr. Ligorio’s previous areas of study at Harvard.

Dr. Ligorio’s patient-centered approach, which is rooted in his training as a general surgeon, is one of the reasons he was recruited to UTSW with the help of multimillion-dollar grants from the Cancer Prevention and Research Institute of Texas. CPRIT’s goal is to support the “most creative ideas and the most meritorious projects” from the cancer research community in Texas.

“This research opens the door to new strategies for treating patients at their most vulnerable stage,” Dr. Timmerman said. “Right now for Stage 4 patients, we’re able to accurately treat nearly any location in the body using highly focused, potent stereotactic ablative radiotherapy. In the past, brain and spinal tumors were the highest priority. By prioritizing tumors adjacent to major blood vessels with a macrovascular component, we can validate Dr. Ligorio’s research and potentially extend patients’ lives.”

The lives behind the research

Megan Wachsmann, M.D., Assistant Professor of Pathology, helped Dr. Ligorio design the rapid autopsy protocols.

A flurry of interest in macrovascular infiltration research has raised expectations for the Ligorio Lab, which makes no secret about its level of ambition. An introductory video on the lab’s website declares: “We’re on a mission to push the boundaries and win the fight against cancer.”

For Dr. Ligorio, that’s not just a platitude. It’s what keeps him up nights and working weekends.

“I’ve put everything into this. It isn’t just another research project,” he said. “There are stories and lives behind this research. My lab is full of emotions because we all know what’s at stake.”

His collaborators are similarly motivated.

Megan Wachsmann, M.D., an Assistant Professor of Pathology at UTSW and staff pathologist at the VA North Texas Health Care System, helped Dr. Ligorio refine the rapid autopsy technique that was so crucial to the study’s findings. For her, this research is an extension of a lifelong pursuit.

Dr. Waschsmann’s mother was diagnosed with pancreatic cancer at age 36.

“As a 9-year-old, that was the defining moment in my development. I’ve spent my training and my career trying to understand ‘the why’ behind cancer deaths so one day I could change it,” she said. “Sometimes in medicine we just accept that things are the way they are. I don’t want to accept that. Neither does Matteo or Kelley. We have the right people coming together at the right time, and that is the beauty of this study.”

Giada Pontecorvi, Ph.D., who came to UT Southwestern from Rome as a postdoctoral researcher in 2022 after winning a fellowship award from the American-Italian Cancer Foundation, can’t imagine a more exhilarating research environment.

Giada Pontecorvi, Ph.D., an Assistant Professor of Surgery, said the Ligorio Lab is studying cancer at its most critical stage.

“We are studying the disease at its most critical stages,” said Dr. Pontecorvi, now an Assistant Professor of Surgery at UTSW. “Being part of a team that is finding fresh answers to fundamental questions about cancer biology – and doing it in a way that keeps patients at the center – has been incredibly motivating.”

Dr. Newcomer said her initial skepticism has long since given way to determination and hope.

“I’m probably even more optimistic than Dr. Ligorio at this point,” she said. “We still have a lot of legwork to do. But I think we are moving toward a scenario where cancer could become more of a chronic disease – where Stage 4 isn’t the death sentence we view it as now.”

She points to HIV as a recent example of how quickly care can evolve. When she began working in hospice, HIV patients made up much of her caseload. Today, she almost never sees them thanks to advances in research and the development of effective drug regimens.

“We may not be able to cure cancer,” she said, “but if we can prevent Stage 5, we can help people live a lot longer and better lives.”

 Dr. Ligorio admits the quest to revolutionize cancer care comes with a deep sense of responsibility.

“I don’t want to instill false hope,” he said. “In the clinical trial, we’re going to be asking hundreds of people to take a different course of treatment for their cancers. These are not mice or organoids; they are humans with families and hopes and dreams.

“So I feel responsible to take this to a different level,” he said, turning to the supplemental portion of his nearly 70-page Nature Medicine study. As he points to a set of images showing tumor emboli in Patient 14’s inferior vena cava wall, his voice quavers.

“She wanted to make an impact. To spare at least one other person from going through what she did,” he said. “If we can do that, this will all have been worth it.”

Dr. Timmerman holds the Effie Marie Cain Distinguished Chair in Cancer Therapy Research and is a member of the Simmons Cancer Center. Dr. Wachsmann is also a member of the Simmons Cancer Center. 

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 16, 2026 – Scientists at Children’s Medical Center Research Institute at UT Southwestern (CRI) have discovered why babies born with a rare inborn error of metabolism, called GPT2 deficiency, suffer from severe neurological impairment, according to research published in Science.

Using their newly developed biosensor to track essential metabolite alpha-ketoglutarate (αKG), researchers found that mitochondrial enzyme GPT2 and transporter protein SLC25A11 work together to control production and transport of αKG from the mitochondria to the nucleus.

This artist rendering depicts the production and transfer of αKG from the mitochondrial matrix to the nucleocytosolic compartment by sequential activities of GPT2 and SLC25A11. (Illustration credit: Melissa Logies for CRI)

Since αKG is essential to unwind DNA for gene transcription, this new research suggests αKG supplementation at birth might help diminish disease progression, according to study leader Samuel McBrayer, Ph.D., Assistant Professor at CRI and of Pediatrics.

“GPT2 is expressed throughout the body, so it was difficult to understand why this enzyme would have a special role in the brain,” Dr. McBrayer said. “The disruption of GPT2 activity causes substantial changes in DNA structure, most profoundly in brain cells, which dysregulates many important genes that must turn on during brain development.”

Based on this insight, Dr. McBrayer collaborated with Eric M. Morrow, M.D., Ph.D., Mencoff Family Professor of Biology at Brown University, whose lab studies GPT2 deficiency and has created a mouse model to investigate the inborn error of metabolism.

More than a decade ago, Dr. Morrow initially characterized metabolic aspects of GPT2 deficiency with the help of Ralph J. DeBerardinis, M.D., Ph.D., Director of the CRI Genetic and Metabolic Disease Program and the Eugene McDermott Center for Human Growth and Development at UT Southwestern.

Using Dr. Morrow’s model, scientists found that by supplementing αKG from birth, newborn mice lacking the Gpt2 enzyme maintained their body weight, one mortality marker of the disease.

“We are really excited about the possibility of developing treatments, such as potentially dietary supplements, that will help patients,” Dr. Morrow said. “The discoveries in this paper provide important new insights on mechanisms, and we will continue to test these treatments in animal studies.”

Scientists previously didn’t understand how the pool of nuclear αKG was regulated. Study first author Alex Sternisha, M.D., Ph.D., a former graduate student in the McBrayer Lab, built a biosensor using a protein from cyanobacteria to examine what creates, transports, or consumes αKG.

“Cyanobacteria evolved this elegant mechanism to sense αKG because it’s so important for their metabolism,” Dr. Sternisha said. “We took a transcription factor that recognizes αKG from cyanobacteria, modified it to function in human cells, and linked its activity to expression of a green fluorescent protein so that we could monitor αKG levels in the nucleus of a living human cell.”

Dr. McBrayer said αKG plays a dual role in cell metabolism. In addition to being part of the mitochondrial TCA cycle – a series of chemical reactions used to produce energy in the cell – it’s also used by chromatin in the nucleus to control how tightly DNA is compacted.

Researchers, including co-first author Haocheng Li, B.S., found that if the GPT2 enzyme doesn’t produce αKG in the mitochondria or if the SLC25A11 protein doesn’t transport it to the cytosol, then not enough αKG diffuses into a cell’s nucleus to support DNA unwinding, affecting DNA access and reducing gene activation.

The study also confirms the enzyme BCAT1, found in the cytosol, is an important αKG consumer and competes with other enzymes for available αKG.

Before now, scientists had only a partial understanding of why GPT2 deficiency leads to fewer synapses and weaker brain circuits. This contributes to neurological symptoms, including severe intellectual disabilities and progressive motor dysfunction, according to the National Organization for Rare Disorders.

“There’s a high degree of hope that we might be able to employ this treatment strategy in patients and really move the needle in that disease context,” Dr. McBrayer said. “Together with Dr. Morrow’s group, we nominated a metabolite supplementation strategy that might prevent some of the defects in neurodevelopment that afflict patients with GPT2 deficiency. We are currently analyzing this treatment strategy with the intent to advance it to clinical trial.”

Dr. McBrayer is an Investigator in the Peter O’Donnell Jr. Brain Institute and a member of the Cellular Networks in Cancer Research Program at the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He is also a Cancer Prevention and Research Institute of Texas (CPRIT) Scholar. He was honored with a Distinguished Scientist Award in 2021 from the Sontag Foundation.

Other study contributors include Dr. DeBerardinis, also Professor of Pediatrics and Director of the CRI Metabolomics Shared Facility; Laura A. Banasyznski, Ph.D., Associate Professor in the Cecil H. and Ida Green Center for Reproductive Biology Sciences, CRI, and Obstetrics and Gynecology; Michalis Agathocleous, Ph.D., Assistant Professor in CRI and Pediatrics; Thomas P. Mathews, Ph.D., Assistant Professor of Research in CRI and Pediatrics, and Assistant Director of the CRI Metabolomics Shared Facility; Chad A. Brautigam, Ph.D., Professor of Biophysics and Microbiology; Yoon Jung Kim, Ph.D., Assistant Professor of Research in CRI and Pediatrics; Javier Garcia-Bermudez, Ph.D., Assistant Professor in CRI and Pediatrics; Lin Xu, Ph.D., Assistant Professor of Health Data Science and Biostatistics in the Peter O’Donnell Jr. School of Public Health and Pediatrics; and Ruth Gordillo, Ph.D., Associate Professor of Internal Medicine.

This research was funded by the National Institutes of Health, the National Cancer Institute, the National Institute of Neurological Disorders and Strokes, the National Institute of General Medicine, the National Institute of General Medical Sciences, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute of Child Health and Human Development, the National Institute on Aging, a CPRIT grant, The Sontag Foundation, the Jonesville Foundation, The Nick Gonzales Foundation for Brain Tumor Research, a Burroughs Wellcome Fund Career Award for Medical Scientists, a Lubin Family Foundation Scholar Award, the Human Frontier Science Program, the American Cancer Society, a Pew-Stewart Scholars for Cancer Research award, The Welch Foundation, and the Howard Hughes Medical Institute Investigator Program.

Dr. DeBerardinis holds the Eugene McDermott Distinguished Chair for the Study of Human Growth and Development and the Philip O’Bryan Montgomery, Jr., M.D. Distinguished Chair in Developmental Biology and is a Sowell Family Scholar in Medical Research.

About CRI

Children’s Medical Center Research Institute at UT Southwestern (CRI) is a joint venture of UT Southwestern Medical Center and Children’s Medical Center Dallas. CRI’s mission is to perform transformative biomedical research to better understand the biological basis of disease. Located in Dallas, Texas, CRI is home to interdisciplinary groups of scientists and physicians pursuing research at the interface of regenerative medicine, cancer biology, and metabolism – relentless discovery toward the treatments of tomorrow.
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About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 13, 2026 – A metabolic byproduct formed when gut bacteria break down dietary fiber appears to protect against dangerous fungal infections common in immunocompromised patients, a study led by UT Southwestern Medical Center researchers shows. The findings, published in Cell Host & Microbe, could lead to new therapies to shield this vulnerable population from Candida albicans, a leading human fungal pathogen.

Andrew Koh, M.D., is Professor of Pediatrics, in the Harold C. Simmons Comprehensive Cancer Center, and of Microbiology. He is also Division Chief of Pediatric Hematology and Oncology at UT Southwestern. He holds the Grant A. Dove Distinguished Chair for Research in Oncology.

“Patients undergoing cancer therapy, stem cell transplantation, cellular therapy, or prolonged antibiotic treatment frequently experience disruption of their gut microbiome and are at increased risk for invasive fungal infections. By identifying specific microbiota-derived metabolites associated with fungal control, this work provides a foundation for developing dietary, microbiome-based, or metabolite-based therapeutic approaches to restore colonization resistance in high-risk patients,” said study leader Andrew Koh, M.D., Professor of Pediatrics, in the Harold C. Simmons Comprehensive Cancer Center, and of Microbiology. He is also Division Chief of Pediatric Hematology and Oncology at UT Southwestern.

Like virtually all animals, humans have a microbiome – a collection of microorganisms that live on and inside the body, particularly in the intestines. This community of bacteria, fungi, archaea, and viruses typically exists in a harmonious balance, with “good” microbes keeping pathogenic ones in check. However, people whose intestinal microbiome has been disrupted through a variety of immunocompromising conditions can lose this equilibrium. This imbalance can cause C. albicans – a normal part of the microbiome – to become overly prominent, leading to sometimes deadly fungal infections.

In 2015, the Koh Lab found that certain good bacteria appeared to stimulate cells in the intestinal lining to produce a natural antibiotic that provides some protection from C. albicans infections. But whether these bacterial species fight off C. albicans through other mechanisms was unknown.

In the new study, Dr. Koh, his longtime collaborator Lora Hooper, Ph.D., Chair and Professor of Immunology and Professor in the Center for the Genetics of Host Defense and Microbiology, and their colleagues looked for common features of these good bacterial species that keep C. albicans in check. They discovered that all of them produce short-chain fatty acids (SCFAs), lipids primarily made as a byproduct of bacterial digestion of dietary fiber.

Antibiotics can disrupt beneficial gut bacteria and the protective metabolites they produce, allowing disease-causing fungi such as Candida albicans to overgrow. Restoring these bacteria-derived metabolites helps re-establish the gut's natural defenses against fungal infection.

When the researchers dosed C. albicans growing in petri dishes with three of these SCFAs – butyric acid, propionic acid, and acetic acid – either alone or together, they found that fungal growth reduced proportionately with increasing SCFA concentrations. Butyric and propionic acids were significantly better at inhibiting C. albicans compared with acetic acid.

Searching for a mechanism, the team compared gene activity in C. albicans cells treated with SCFAs and those left untreated. Results showed that the SCFAs impaired uptake of glucose, a major nutrient for C. albicans; disrupted its ability to digest glucose and other nutrients; and caused the fungal cell interiors to become more acidic. Each of these suppressed pathways led metabolism and growth of C. albicans to slow or shut down, preventing it from overtaking other gut microorganisms.

When the researchers treated mice colonized with C. albicans with SCFAs, they found that this intervention was far more successful in mice with typical intestinal microbiomes than in “germ-free” mice without these bacteria. A closer look showed that the SCFAs encouraged the growth of good bacteria that make these lipids, compounding their anti-fungal effects. When the researchers colonized mouse intestines with bacteria altered to prevent SCFA production, the delivered SCFAs weren’t as effective against C. albicans infections.

The scientists then developed a chemical construct that tied a type of dietary fiber called inulin to propionic acid, which released this SCFA after bacterial digestion in the large intestine, where C. albicans primarily resides. The treatment significantly reduced the amount of this fungus in mouse intestines, suggesting that a similar intervention might be effective in humans as well.

The team plans to continue studying how SCFAs fight C. albicans infections.

A complete list of UTSW authors can be found in the study.

Dr. Koh holds the Grant A. Dove Distinguished Chair for Research in Oncology. He is also a member of the Development and Cancer Research Program at Simmons Cancer Center. Dr. Hooper holds the Jonathan W. Uhr, M.D. Distinguished Chair in Immunology and is a Nancy Cain and Jeffrey A. Marcus Scholar in Medical Research, in Honor of Dr. Bill S. Vowell. She is a member of the Cellular Networks in Cancer Research Program at Simmons Cancer Center.

This research was funded by a grant from the National Institute of Allergy and Infectious Diseases (P01AI179406) and a National Cancer Institute (NCI) Cancer Center Support Grant (P30CA142543).

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 08, 2026 – Treating glioblastoma with a class of drugs known as EGFR inhibitors made this cancer more sensitive to chemotherapy, suggests a study in preclinical models co-led by researchers at UT Southwestern Medical Center and the University of Alabama at Birmingham. The findings, published in Science Translational Medicine, could lead to a new strategy for fighting the most common primary brain cancer in adults.

Amyn Habib, M.D., is Professor of Neurology and Neurological Surgery at UT Southwestern and a Staff Physician at the Dallas Veterans Affairs Medical Center. Dr. Habib is also a member of the Development and Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center and an Investigator in the Peter O’Donnell Jr. Brain Institute.

“Glioblastoma is a devastating brain cancer with a dismal prognosis and no truly effective treatments. Our study could give new hope to the approximately 250,000 patients worldwide diagnosed with this disease each year,” said Amyn Habib, M.D., Professor of Neurology and Neurological Surgery at UT Southwestern and Staff Physician at the Dallas Veterans Affairs Medical Center. Dr. Habib is also a member of the Development and Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center and an Investigator in the Peter O’Donnell Jr. Brain Institute.

Dr. Habib co-led the study with Gao Guo, D.D.S., M.S.D., Ph.D., Assistant Professor of Neurosurgery at the University of Alabama at Birmingham and a former postdoctoral researcher in the Habib Lab. The co-first authors of the study are Arifa Nayab, M.P.H., a former member of the Habib Lab, and Nouman Mughal, Ph.D., former Assistant Professor of Surgery at Aga Khan University in Pakistan.

Despite decades of research, outcomes for glioblastoma remain grim: Most patients survive 12 to 18 months after diagnosis, with five-year survival rates at 5%-7%. Along with surgery and radiation, glioblastoma is typically treated with the chemotherapy agent temozolomide (TMZ). This drug works by damaging the DNA of cancer cells, preventing them from dividing and eventually causing their death. However, glioblastoma patients who initially respond to TMZ almost inevitably develop incurable drug-resistant cancer in the brain. There are no effective treatments for recurrent, TMZ-resistant glioblastoma.

Researchers have long known that TMZ is most effective for tumors that don’t produce a protein called O-6-methylguanine-DNA methyltransferase (MGMT), which repairs the DNA damage caused by TMZ. But because TMZ has been shown to increase MGMT over time, Dr. Habib explained, understanding how cells regulate this process could lead to more effective treatments for glioblastoma.

The Habib Lab has a long-standing focus on how the epidermal growth factor receptor (EGFR), a protein produced by a gene frequently mutated in glioblastoma, drives this and several other types of cancer. While studying what molecular pathways are influenced by EGFR, Dr. Habib and his colleagues discovered that inhibiting EGFR also significantly reduced the amount of MGMT produced by glioblastoma cells growing in the laboratory. They found a similar effect in mouse models of glioblastoma.

Additional experiments showed that an EGFR inhibitor called afatinib also made glioblastoma cells and tumors growing in mice more sensitive to TMZ, even when they had developed TMZ resistance. However, this strategy only worked when the researchers pretreated with afatinib a day before they delivered TMZ. Giving both drugs simultaneously had no effect, Dr. Habib said, since MGMT production must be shut down through EGFR inhibition before TMZ can do its job.

This finding may explain why clinical trials testing TMZ and EGFR inhibitors delivered together haven’t had success, Dr. Habib added. When the researchers examined glioblastoma samples from patients who participated in one such trial, they found that the tumor cells had high levels of MGMT that prevented TMZ from working. Glioblastoma samples from a different clinical trial testing only a novel EGFR inhibitor showed significantly reduced MGMT levels, suggesting that TMZ may be effective after administration of the EGFR-targeted drug.

If future clinical trials confirm that treatment with EGFR inhibitors sensitizes glioblastoma patients to TMZ, this strategy could eventually become the gold standard for treating this cancer, Dr. Habib said.

A complete list of UTSW contributors can be found in the study. 

This research was funded by grants from the National Institutes of Health (R01CA299152-01 and 1R01NS119225-01A1) and the National Cancer Institute Cancer Center Support Grant (P30CA142543).

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 07, 2026 – Scientists at UT Southwestern Medical Center have discovered that gut bacteria help regulate the development of the body’s immune system by directing the movement of vitamin A through a previously unrecognized cellular network. The preclinical findings, published in Cell Host & Microbe, could reshape how researchers view conditions in which immune development is disrupted, highlighting nutrient pathways as potential targets for therapeutic intervention.

Tarun Srinivasan, Ph.D., is a third-year medical student in UT Southwestern’s Perot Family Scholars Medical Scientist Training Program.

“We’ve known for years that both gut microbes and vitamin A are important for building a healthy immune system,” said first author Tarun Srinivasan, Ph.D., a third-year medical student in UT Southwestern’s Perot Family Scholars Medical Scientist Training Program entering his third year of medical school. “What we didn’t understand was how those two were connected. This study identifies the pathway that links them.”

The study’s co-corresponding authors are Lora Hooper, Ph.D., Chair and Professor of Immunology and Professor in the Center for the Genetics of Host Defense and of Microbiology, and Andrew Koh, M.D., Professor of Pediatrics, Chief of the Division of Pediatric Hematology and Oncology, and Professor of Microbiology. Both are members of the Harold C. Simmons Comprehensive Cancer Center.

The immune system relies on vitamin A-derived signals to guide the development of T cells, a class of immune cells that protects the body from infection. Researchers have long known both vitamin A and the gut microbiome are essential for immune development, but exactly how these factors work together has remained unclear.

UTSW scientists found that gut bacteria in mice trigger a stepwise transfer of vitamin A between cells. The process begins in the intestinal lining, where microbes stimulate production of a vitamin A-binding protein called serum amyloid A (SAA). SAA delivers vitamin A to immune cells in the intestine, which then carry it to nearby lymph nodes and pass vitamin A-derived signals to developing T cells.

Lora Hooper, Ph.D., is Chair and Professor of Immunology and Professor in the Center for the Genetics of Host Defense and of Microbiology at UT Southwestern. She is a member of the Harold C. Simmons Comprehensive Cancer Center.

When gut bacteria were removed, this vitamin A delivery system was largely shut down, leaving developing T cells unable to mature properly or migrate to the intestine. Because these steps are essential for building a functional immune defense, disruptions in this pathway could impair the body’s ability to respond to infections or maintain normal immune balance. Researchers further showed this pathway became increasingly active during early life – a critical window when the immune system is being programmed – suggesting interruptions during this period could have lasting consequences.

Together, this work shows gut microbes are not just passive residents – they actively control how a key nutrient signal reaches the cells that build the immune system.

Study authors said the findings may help explain how antibiotic exposure during early life influences immune development. Because the newly identified pathway depends on signals from gut microbes, disruptions in the microbiome could interfere with how vitamin A-derived signals are delivered to the developing immune cells. Understanding this process may help explain links between early-life microbiome disruption and increased risk of infections, inflammatory conditions, or poor immune regulation later in life.

“One of the long-standing mysteries in the field has been how the gut microbiome communicates with the developing immune system,” Dr. Hooper said. “Our study shows vitamin A is a key part of that conversation. It’s exciting because it reveals how gut microbes and nutrients from the diet work together to help build a healthy immune system early in life.”

Andrew Koh, M.D., is Professor of Pediatrics, Chief of the Division of Pediatric Hematology and Oncology, and Professor of Microbiology at UT Southwestern. He is a member of the Harold C. Simmons Comprehensive Cancer Center.

The findings reveal gut microbes do more than simply stimulate immune cells. They also control how a key nutrient-derived developmental signal is distributed throughout the immune system.

This research suggests immune development may depend not only on the availability of nutrients such as vitamin A, but also on the body’s ability to deliver those nutrients to the right immune cells at the right time.

“These findings point to vitamin A signaling as a potentially actionable way to tune immune responses,” Dr. Koh said. “From a translational standpoint, that raises the possibility that carefully modulating this pathway could one day help improve the balance between efficacy and toxicity in cancer immunotherapy.”

A complete list of authors from UTSW can be found in the study.

This study was supported by grants from the National Institutes of Health (R01 DK070855, R01 CA231303, P01 AI179406, T32 AI007520) and The Welch Foundation (I-1874); the Walter M. and Helen D. Bader Center for Research on Arthritis and Autoimmune Diseases; the UT Southwestern and Children’s Health Cellular and ImmunoTherapeutics Program (CITP); the Howard Hughes Medical Institute; and the National Cancer Institute Cancer Center Support Grant (P30CA142543).

Dr. Hooper holds the Jonathan W. Uhr, M.D. Distinguished Chair in Immunology. Dr. Koh holds the Grant A. Dove Distinguished Chair for Research in Oncology.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – July 06, 2026 – UT Southwestern Medical Center is ranked No. 1 among healthcare institutions worldwide by Nature Index for publishing high-quality research in all subjects for the 12-month period that ended Feb. 28, 2026. UTSW also ranked No. 1 among healthcare institutions globally for research in the natural sciences and biological sciences.

Joan Conaway, Ph.D., is Vice Provost and Dean of Basic Research at UT Southwestern and holds the Cecil H. Green Distinguished Chair in Cellular and Molecular Biology.

Nature Index tracks healthcare research articles published in top science journals, offering a snapshot of high-quality discoveries from 6,545 institutions around the world. For UTSW during the ranking period, that included more than 500 research papers published in nearly 100 journals, ranging from Nature and Science to Circulation and The Journal of the American Medical Association. The work spans studies tracking the effects of GLP-1 medications, reprogramming heart cells to restore function after a heart attack, identifying fibroblast populations that drive cancer progression, revealing how different parts of the hippocampus in the brain support memory, and more.

“This ranking reflects the depth and excellence of our research enterprise,” said Joan Conaway, Ph.D., Vice Provost and Dean of Basic Research at UT Southwestern, who holds the Cecil H. Green Distinguished Chair in Cellular and Molecular Biology. “Our scientists are working at the highest level to advance knowledge across disciplines to better understand diseases and translate those insights into meaningful progress for patients.”

In addition, UT Southwestern ranked first during the same period among 1,192 healthcare institutions in North America and 995 entities in the United States.

W. P. Andrew Lee, M.D., is Executive Vice President for Academic Affairs, Provost, and Dean of UT Southwestern Medical School and holds the Atticus James Gill, M.D. Chair in Medical Science.

“This recognition highlights the sustained efforts of our faculty and trainees,” said W. P. Andrew Lee, M.D., Executive Vice President for Academic Affairs, Provost, and Dean of UT Southwestern Medical School, who holds the Atticus James Gill, M.D. Chair in Medical Science. “By supporting rigorous research and collaboration, we’re able to translate discoveries into real-world impact.”

With more than 1 million square feet of research space, UT Southwestern supports about 6,200 research projects a year and receives more than $816 million in annual funding from state and federal agencies as well as individuals and corporations.

Its portfolio includes the Harold C. Simmons Comprehensive Cancer Center and the Peter O’Donnell Jr. Brain Institute as well as one of only 11 Nutrition Obesity Research Centers in the country and a National Organization for Rare Disorders (NORD) Rare Disease Center of Excellence. UTSW also is designated as a National Cancer Institute Specialized Program of Research Excellence (SPORE) site in liver cancer, lung cancer, and kidney cancer.

Among many research honors, six UT Southwestern faculty members have been awarded the Nobel Prize, and three have received the Breakthrough Prize in Life Sciences. In addition, five faculty members have received the Albert Lasker Basic Medical Research Award – considered the country’s preeminent biomedical research award – including Steven McKnight, Ph.D., Professor of Biochemistry, in 2025 and Zhijian “James” Chen, Ph.D., Professor of Molecular Biology and in the Center for the Genetics of Host Defense, in 2024.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 28 members of the National Academy of Sciences, 26 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – June 30, 2026 – A team at UT Southwestern Medical Center is the first in North Texas to offer single-port robotic-assisted thoracoscopic lobectomy, a minimally invasive procedure for select patients with early-stage lung cancer.

Takashi Eguchi, M.D., Ph.D., is Assistant Professor of Cardiovascular & Thoracic Surgery at UT Southwestern.

Since March, UT Southwestern surgeons have performed 13 single-port pulmonary resections, including lobectomies and segmentectomies, using a single-port robotic surgical system (da Vinci SP). The system received Food and Drug Administration clearance in 2024 for certain urologic and thoracoscopic procedures. The platform allows surgeons to remove tumors and surrounding tissue through a single inch-long incision below the rib cage.

“Our goal is to provide patients with lung cancer an efficient, complete, and timely treatment pathway. Adopting this new technology is a welcome extension of our comprehensive thoracic oncology program,” said Takashi Eguchi, M.D., Ph.D., Assistant Professor of Cardiovascular & Thoracic Surgery at UT Southwestern.

Dr. Eguchi and Aitua Salami, M.D., M.P.H., Assistant Professor of Cardiovascular & Thoracic Surgery and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern, perform this unique surgery.

UT Southwestern thoracic surgeons use advanced imaging techniques such as near-infrared technology and 3D reconstruction to localize lung nodules that may not be visible with traditional white light imaging so that they are amenable to precise lung resections.

Aitua Salami, M.D., M.P.H., is Assistant Professor of Cardiovascular & Thoracic Surgery and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

“When we see patients with suspicious lung nodules, we implement an accelerated treatment pathway,” Dr. Salami said. “In some cases, we can move patients from nodule identification to definitive treatment within a few days, compared to several weeks or months at lower-volume centers.”

For select patients with early-stage lung cancer, the single-port technique may facilitate earlier recovery, shorter hospital stays, reduced pain, and a lower risk of certain postoperative complications.

“Patients may experience less pain after single-port robotic resection because we access the lung below the rib cage instead of through the chest,” Dr. Salami said.

In most cases, lung cancer is highly treatable when diagnosed at an early stage and managed by a multidisciplinary team.

“At UT Southwestern, thoracic surgery, interventional pulmonology, medical and radiation oncology are integrated into one team, ensuring that every patient gets an individualized treatment plan,” Dr. Eguchi said. “Offering single-port lobectomy expands our treatment options and supports our goal of delivering precise, individualized care.”

UT Southwestern is ranked among the top 20 hospitals nationwide for cardiology, heart & vascular surgery and for pulmonology & lung surgery by U.S. News & World Report.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – June 29, 2026 – An RNA-modifying enzyme linked to cancer and neurological disorders selects its targets by recognizing specific RNA shapes and sequences, according to a study by UT Southwestern Medical Center researchers. The findings, published in Nature, define the molecular features that guide the enzyme, NSUN2, to the RNAs it modifies and could help researchers investigate how abnormal RNA modification contributes to disease.

“NSUN2 is an oncogenic RNA modification enzyme, and we discovered how it recognizes targets, including what elements constitute the target RNAs,” said corresponding author Yunsun Nam, Ph.D., Professor of Biochemistry and Biophysics at UT Southwestern. Dr. Nam is also a member of the Harold C. Simmons Comprehensive Cancer Center and an Investigator in the Peter O’Donnell Jr. Brain Institute. Jacob Canepa, B.S., graduate student researcher in the Nam Lab, was the study’s first author.

A 3D view shows the cancer-linked enzyme NSUN2 interacting with tRNA (orange), a molecule vital for building proteins. The transparent colored surfaces highlight different sections of the enzyme. Cyan marks the exact spot on the RNA being altered, and a helper molecule is shown in pink.

RNA helps cells interpret and use genetic information. Like DNA and proteins, RNA can be chemically modified in ways that influence its function, stability, and fate inside cells. NSUN2 is one of the enzymes that writes those marks, adding a modification known as 5-methylcytosine (m5C) to several types of RNA.

But NSUN2 has been difficult to understand because it can modify many different RNAs, and previous studies had not determined how the enzyme chooses its targets. That uncertainty has limited efforts to understand how NSUN2 contributes to disease. NSUN2 is overexpressed in many types of cancer, especially lung cancer, and mutations in the gene that encodes NSUN2 have been linked to intellectual disabilities, including Dubowitz-like syndrome.

To define how NSUN2 selects its targets, the Nam Lab worked with UTSW’s Cryo-Electron Microscopy Facility to capture multiple 3D structures of NSUN2 bound to RNA at different stages of methylation, a chemical modification cells can make to RNA. These structures showed that NSUN2 recognizes RNA through a combination of shape and sequence. In particular, the enzyme prefers RNAs with two stemlike regions arranged in a specific orientation, along with a short sequence pattern near the modification site.

The researchers then tested those structural findings through biochemical experiments, including designing a shortened RNA molecule that retained the essential features needed for NSUN2 recognition. The results allowed them to define the necessary and sufficient features that make an RNA molecule a direct target of NSUN2. 

The work also revealed an unexpected view of transfer RNA (tRNA), one of the most abundant types of RNA in cells. When bound to NSUN2, tRNA adopted a shape that differed from its classic L-shaped structure, suggesting this familiar molecule can take on more dynamic forms than previously realized.

“Our findings close this gap by identifying the specific molecular targets that NSUN2 acts on – knowledge that opens new directions for studying how this protein disrupts normal gene expression and contributes to disease including cancer,” Dr. Nam said. “Importantly, these results also lay the groundwork for developing therapies that directly target NSUN2 and its downstream effects.” 

The study builds on previous work from the Nam Lab published in 2023 and 2024 showing that RNA-modifying enzymes can act on different substrates with varying efficiency. Understanding those differences is especially important in cancer, where overexpressed enzymes may begin modifying RNAs they would normally affect only weakly or inadvertently.

Other UTSW researchers in the Nam Lab who contributed to this study are Victor Ruiz-Arroyo, Ph.D., postdoctoral research fellow, and Netanya Schlamowitz, B.A., graduate student researcher.

Dr. Nam holds the Doris and Bryan Wildenthal Distinguished Chair in Medical Science and is a Southwestern Medical Foundation Scholar in Biomedical Research and a UT Southwestern Presidential Scholar. Dr. Nam received the 2026 Edith and Peter O’Donnell Award in Biological Sciences from the Texas Academy of Medicine, Engineering, Science & Technology (TAMEST) for her research into how RNAs and proteins interact at the molecular level. 

This study was funded by grants from the National Institutes of Health (R01GM122960, R01CA258589, R01ES038329, and T32GM131963), the American Cancer Society (PF-24-1308804-01-RMC), The Welch Foundation (I-2115-20220331), the Cancer Prevention and Research Institute of Texas (RP210041), and the National Cancer Institute (NCI) Cancer Center Support Grant (P30CA142543).

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – June 24, 2026 – The widespread use of electronic patient portals to provide quick access to test results presents healthcare professionals with an important challenge: How should new cancer diagnoses be communicated?

An increasing number of patients are learning about new or recurrent cancer diagnoses through their portals – a direct result of a provision in the 21st Century Cures Act, implemented in 2021. That regulation mandates that patients have timely, unrestricted access to their electronic health information.

Sheena Bhalla, M.D., is Assistant Professor of Internal Medicine in the Division of Hematology and Oncology and a medical oncologist at the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

But a new survey conducted at UT Southwestern Medical Center has found that most cancer patients would still prefer to learn results directly from their doctors. 

“While most patients in the general population appreciate rapid electronic access to test results, the situation for patients with cancer is much more nuanced,” said the study’s lead author, Sheena Bhalla, M.D., Assistant Professor of Internal Medicine in the Division of Hematology and Oncology and a medical oncologist at the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. “Learning about a cancer diagnosis without the ability to immediately ask questions or discuss next steps with a trusted clinician can add to the significant stress, uncertainty, and fear that patients experience.”

The survey results, published in JAMA Network Open, found that 75% of patients would prefer to find out about a cancer diagnosis directly from their physician, either in person or via a telemedicine appointment. The 2025 survey collected responses from more than 2,400 patients diagnosed with cancer at Simmons Cancer Center between 2019 and 2023.

Patient preferences varied based on prior experiences, frequency of portal use, and demographic characteristics. For example, men were more likely to prefer learning about a diagnosis via the portal.

David Gerber, M.D., is Professor of Internal Medicine in the Division of Hematology and Oncology and of Epidemiology in the Peter O'Donnell Jr. School of Public Health and co-Director of the Simmons Cancer Center Office of Education and Training.

“These findings highlight the need for a more personalized, tailored approach to communicating sensitive and life-changing results,” said study senior author David Gerber, M.D., Professor of Internal Medicine in the Division of Hematology and Oncology and of Epidemiology in the Peter O'Donnell Jr. School of Public Health and co-Director of the Simmons Cancer Center Office of Education and Training. “Moving beyond a one-size-fits-all approach can help clinicians provide a more thoughtful, compassionate patient experience.”

The study also provided insight into the real-world circumstances by which patients are receiving sensitive results, with more than half of those who learned of their diagnosis via the portal reporting they were alone at the time.

“That’s one of the most unintended consequences of real-time access,” Dr. Bhalla said. “Patients are often alone without support from their physician or family at one of their most vulnerable moments.”

The researchers say healthcare providers have several potential solutions, including improving clinician and patient awareness of available portal notification settings; developing tiered or delayed-release approaches for particularly sensitive findings; and integrating supportive digital tools such as plain-language summaries for radiology and pathology reports. In addition, since the implementation of the Cures Act, three states, including Texas, have enacted laws that allow delayed portal release of cancer-related and other sensitive results. 

“Further study and increased interdisciplinary collaboration among oncology clinicians, health services researchers, and digital health experts can help us better understand how patients receive and react to cancer diagnoses,” Dr. Bhalla said. “Our goal is to increase awareness of this issue and help drive innovative approaches to patient-centered communication.”

Other UTSW researchers who contributed to this study are Song Zhang, Ph.D., Professor and Interim Vice Chair of Health Data Science and Biostatistics in the O'Donnell School of Public Health; Meera J. Patel, Ph.D., Assistant Professor of Social and Behavioral Sciences in the O'Donnell School of Public Health; Heather Kitzman, Ph.D., Adjunct Associate Professor of Social and Behavioral Sciences in the O'Donnell School of Public Health as well as Chief Research Officer at Parkland Health; Jeremy Louissaint, M.D., M.S.H.I., Assistant Professor of Internal Medicine in the Division of Digestive and Liver Diseases; Alana Christie, M.S., Biostatistical Consultant; Ruchira Garg, M.S., Business Operations Analyst; Lauren Abruzzo, Ph.D., medical student; and Donglu Xie, M.S., Senior Programmer, Information Resources Enterprise Data Services. 

Dr. Gerber holds the David Bruton, Jr. Professorship in Clinical Cancer Research. Dr. Bhalla serves as Director of Thoracic Medical Oncology Clinical Operations at Simmons Cancer Center.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – June 15, 2026 – Belzutifan, a first-in-class drug that arose from scientific discoveries at UT Southwestern Medical Center, has been approved by the Food and Drug Administration to treat some patients with earlier stage kidney cancers in combination with an immunotherapy drug. This move marks the latest expansion of belzutifan’s indications after it was originally approved in 2021.

Hans Hammers, M.D., Ph.D., is Professor of Internal Medicine in the Division of Hematology and Oncology, co-leader of the Experimental Therapeutics Research Program in the Harold C. Simmons Comprehensive Cancer Center, and co-leader of clinical research and immunotherapy in UTSW’s Kidney Cancer Program.

The latest FDA approval was based on results from LITESPARK-022, a phase three clinical trial that took place at 285 sites around the world, including UT Southwestern. The results, presented at the 2026 ASCO Genitourinary Cancer Symposium, evaluated belzutifan combined with pembrolizumab – a type of immunotherapy drug known as a checkpoint inhibitor – in patients with clear cell renal cell carcinoma after surgery to remove diseased kidneys. At a median follow-up of 28.4 months, results showed that this combination reduced the risk of disease recurrence by 28% compared with pembrolizumab with a placebo.

“LITESPARK-022 demonstrated an improvement in disease-free survival by 28% when belzutifan was combined with pembrolizumab in patients with higher risk for kidney cancer recurrence,” said Hans Hammers, M.D., Ph.D., Professor of Internal Medicine in the Division of Hematology and Oncology, co-leader of the Experimental Therapeutics Research Program in the Harold C. Simmons Comprehensive Cancer Center, and co-leader of clinical research in UTSW’s Kidney Cancer Program, who served as the site leader for the clinical trial at Simmons Cancer Center. “This trial showed an advance over pembrolizumab monotherapy in this setting, but overall survival was immature at the time of analysis.” 

Belzutifan, which is manufactured by Merck, known as MSD outside of the United States and Canada, previously received regulatory approvals to treat patients with certain von Hippel-Lindau disease-associated tumors (a type of familial kidney cancer); later-stage renal cell carcinoma; and pheochromocytoma or paraganglioma, two types of rare neuroendocrine tumors.

Legacy of discovery

Belzutifan originated from 1990s research at UT Southwestern by Steven McKnight, Ph.D., Professor of Biochemistry, and David Russell, Ph.D., Professor Emeritus of Molecular Genetics, who discovered HIF-2α, the molecular target of belzutifan. Originally known for helping cells adapt to low oxygen, HIF-2α was later found to drive kidney cancer growth. UTSW scientists identified a druggable cavity in the HIF-2α protein and pursued inhibitors that bind to that cavity.

To develop an effective HIF-2α inhibitor, they founded Peloton Therapeutics. Discoveries at Peloton were followed by UTSW-led preclinical studies and first-in-human clinical trials with the drug that later became belzutifan. Merck acquired Peloton in 2019. Merck also manufactures pembrolizumab.

The Kidney Cancer Program at UTSW’s Simmons Cancer Center is one of only two National Cancer Institute-designated Specialized Programs of Research Excellence (SPOREs) in kidney cancer and a global leader in this disease. James Brugarolas, M.D., Ph.D., is the founding Director of the Kidney Cancer Program and Professor of Internal Medicine in the Division of Hematology and Oncology.

Simmons Cancer Center is one of 34 members of the National Comprehensive Cancer Network and one of 58 National Cancer Institute-Designated Comprehensive Cancer Centers. Simmons Cancer Center is ranked in the top 20 centers for cancer care by U.S. News & World Report. Its faculty members treat more than 11,000 new cancer cases a year, participate in over 500 active clinical trials, and have more than $120 million in extramural cancer-focused research funding.

Dr. Hammers is the inaugural Eugene P. Frenkel, M.D. Scholar in Clinical Medicine. Dr. McKnight holds the Distinguished Chair in Basic Biomedical Research. Dr. Brugarolas holds the Sherry Wigley Crow Cancer Research Endowed Chair in Honor of Robert Lewis Kirby, M.D.

UT Southwestern and some of its researchers will receive financial compensation, through prior agreements with Peloton, based on belzutifan’s FDA approval.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – June 11, 2026 – An experimental antibody treatment that binds to a protein known as PCDH7 shrank tumors in preclinical models of non-small cell lung cancer (NSCLC), even those resistant to a targeted therapy, a study led by UT Southwestern Medical Center researchers showed. The findings, published in Science Advances, could eventually lead to a new class of drugs to treat NSCLC and potentially other cancers.

Kathryn O’Donnell, Ph.D., is Associate Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

“Overcoming resistance to molecularly targeted therapies is a critical unmet need for lung cancer patients. We are excited that these antibodies may open another therapeutic avenue for lung cancer, especially for patients whose cancers have become resistant to KRAS inhibitors,” said Kathryn O’Donnell, Ph.D., Associate Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. Dr. O’Donnell co-led the study with first author Nicole Novaresi, Ph.D., a postdoctoral researcher in the O’Donnell Lab, and collaborators at the University of Texas Health Science Center at Houston.

NSCLC accounts for about 85% of lung cancer cases in the U.S. and is the leading cause of cancer-related deaths. The O’Donnell Lab focuses on identifying and characterizing proteins on the surface of NSCLC and other cancer cells due to their potential as therapeutic targets. In 2017, Dr. O’Donnell and her colleagues identified PCDH7 as a driver of NSCLC, especially in tumors with mutations in a gene called KRAS. Found in about 25% of NSCLC cases, these mutations cause uncontrolled cell proliferation that propels tumor growth.

In 2024, the Food and Drug Administration approved a drug called adagrasib, which targets NSCLC with KRAS mutations. However, patients inevitably developed resistance to this treatment over time, leaving them with few therapeutic options.

Nicole Novaresi, Ph.D., is a postdoctoral researcher in the O’Donnell Lab.

Searching for a new way to attack NSCLC, Dr. O’Donnell’s group collaborated with Zhiqiang An, Ph.D., and Ningyan Zhang, Ph.D., at the University of Texas Health Science Center to develop antibodies that target PCDH7. The teams then worked closely to characterize and functionally evaluate them. Starting with hundreds of antibody candidates, the researchers narrowed their focus to an antibody called mAb7 that bound strongly to PCDH7, reduced intracellular signaling and proliferation in NSCLC cells, and eventually caused the cancer cells to die.

When the scientists treated mice growing KRAS-mutant NSCLC tumors with mAb7, the tumors shrank significantly. This effect was enhanced when mAb7 was delivered with a drug called trametinib, which targets MAPK/ERK enzymes in the cancer-promoting RAS pathway. This treatment also sensitized the KRAS-mutant NSCLC tumors to adagrasib, causing an effect that reduced tumor size significantly more than mAb7 or adagrasib alone. The team also found that PCDH7 was upregulated in tumors that eventually developed resistance to adagrasib and that mAb7 reduced the growth of those drug-resistant tumors.

To get a sense of whether this strategy might work in patients, the researchers tested mAb7 on mice engineered to have human immune systems. A closer look showed that the antibodies brought immune cells to the human tumor cells and effectively eliminated the cancer cells.

These novel antibodies will require significant testing before use in patients, Dr. Novaresi said. But eventually, they may be used alone or in combination with adagrasib or other emerging targeted cancer therapies. Enhancing them by attaching chemotherapy drugs or by engaging immune cells could help the antibodies fight NSCLC even more effectively. She added that mAb7 may also have potential for treating additional cancers that produce PCDH7 on their cell surfaces, including pancreatic cancer, melanoma, and prostate cancer.

Other UTSW researchers who contributed to this study are John Minna, M.D., Director of the Hamon Center for Therapeutic Oncology Research, Professor of Internal Medicine and Pharmacology, and co-leader of the Experimental Therapeutics Research Program at Simmons Cancer Center; Chul Ahn, Ph.D., Professor of Health Data Science and Biostatistics and a member of the Population Science and Cancer Control Research Program at Simmons Cancer Center; and Shayna Thomas-Jardin, Ph.D., a postdoctoral researcher in the O’Donnell Lab.

Dr. O’Donnell is co-leader of the Development and Cancer Research Program in the Simmons Cancer Center.

This study was funded by grants from the National Cancer Institute (NCI) (R01 CA207763 and P50CA70907), the Cancer Prevention and Research Institute of Texas (RP250391, RP190610, RP200327, RP250572, RP260660, and RP210041), The Welch Foundation (I-1881), the V Foundation, the Department of Defense (LC190249), the American Lung Association (LCD 1421064), and the NCI Cancer Center Support Grant (P30CA142543).

Dr. O’Donnell is a scientific co-founder and adviser of ProtomAb Therapeutics Inc., a company created to continue this work. The University of Texas System has filed a provisional patent application on the PCDH7 antibodies for cancer care.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – May 21, 2026 – When activated in ovarian cancer cells, the receptor for the body’s primary stress hormone alters the tumor environment in ways that blunt immune response, according to new research led by UT Southwestern Medical Center. The findings, published in Endocrinology, identify a previously unrecognized role for the glucocorticoid receptor (GR) in shaping the ovarian cancer tumor microenvironment.

“Understanding master regulators (like GR) of tumor cell evasion from the immune system could lead to more effective treatment of ovarian cancer – both in combination with chemotherapy and eventually with immunotherapy,” said corresponding author Suzanne Conzen, M.D., Professor of Internal Medicine, Chief of the Division of Hematology and Oncology, and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

Suzanne Conzen, M.D., is Professor of Internal Medicine, Chief of the Division of Hematology and Oncology, and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. She holds the Andrea L. Simmons Distinguished Chair in Cancer Research.

Most ovarian tumors exist in a so-called “cold” state, meaning they attract few immune cells needed to mount an effective attack, but what drives that state has been poorly defined. The Conzen Lab previously found that ovarian cancers with high GR expression are linked to shorter periods of progression-free survival among patients, suggesting the receptor plays an important role in how the disease progresses.

In the new study, the team examined ovarian cancer cells from humans and mice, mouse tumor models, and large databases of patient tumor data. They found that when GR was switched on inside cancer cells, the cells released a mix of chemical signals that summoned immune-suppressing cells into the tumor. Those recruited cells, which are more abundant in patients with worse outcomes, shut down the immune system’s ability to attack the cancer.

When the researchers blocked GR, either with a drug called relacorilant or by genetically removing the receptor from tumor cells, the suppressive signals dropped. Fewer immune-suppressing cells made their way into tumors, and more of the immune cells that fight cancer moved in. 

The findings also align with clinical progress already underway. The Food and Drug Administration recently approved relacorilant combined with nab-paclitaxel for platinum-resistant ovarian, fallopian tube, or primary peritoneal cancer. The phase three trial supporting that approval was based on a series of earlier research from Dr. Conzen and her colleagues showing that GR activity helps ovarian cancer cells survive chemotherapy. The new UTSW findings suggest the drug may also reawaken antitumor immunity.

“Future clinical trials will likely examine whether GR modulation could assist with immunotherapy responses in ovarian cancer,” Dr. Conzen said.

Other UTSW researchers in the Division of Hematology and Oncology who contributed to this study are first author and postdoctoral researcher Manisha Taya, Ph.D.; Tryambak Srivastava, Ph.D., and Woei-Yaw Chee, Ph.D., postdoctoral researchers; Andrew W. DeVilbiss, Ph.D., Instructor; and Lynda Bennett, Ph.D., Assistant Professor.

Dr. Conzen holds the Andrea L. Simmons Distinguished Chair in Cancer Research and is a member of the Experimental Therapeutics Research Program at Simmons Cancer Center.

This study was funded by grants from the National Institutes of Health (CA223426), the Cancer Prevention and Research Institute of Texas (RR1900371), and the National Cancer Institute (NCI) Cancer Center Support Grant (P30CA142543).

Dr. Conzen holds patents through the University of Chicago on methods related to using GR expression in triple-negative breast and prostate cancer prognosis and treatment and has received honoraria from Corcept Therapeutics for advisory board service related to breast cancer. UT Southwestern has a patent application pending on GR transcriptional activity in ovarian cancer.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – May 19, 2026 – Scientists at Children’s Medical Center Research Institute at UT Southwestern (CRI) have discovered that large pieces of DNA can transfer directly between human cells, and the DNA can persist and change how the recipient cell functions. The findings, published today in Cell, challenge a long-standing view that the genomes of individual human cells evolve independently from one another.

The study shows DNA damage and errors in cell division can cause pieces of genomic DNA to escape from the nucleus and move into nearby cells through nanotubes – thin, tubelike structures that briefly form when some cells come into contact.

Once inside a recipient cell, transferred DNA can enter the nucleus and become incorporated into the cell’s genome. Researchers found that transferred DNA persisted through multiple rounds of cell division, remained biologically active, and conferred new traits to recipient cells.

“This was a surprising discovery,” said study leader Peter Ly, Ph.D., Assistant Professor in CRI and of Cell Biology, Pediatrics, and in the Harold C. Simmons Comprehensive Cancer Center. “Our findings suggest neighboring cells may be able to directly reshape one another’s genomes in ways we did not anticipate.” 

Study first author Elizabeth Maurais, Ph.D., a recent graduate of the Genetics, Development and Disease Program at UT Southwestern, and other Ly Lab researchers uncovered this process while studying how cells respond to genomic instability, including DNA damage caused by chemotherapy and radiation treatment.

Live-cell microscopy shows a DNA-containing micronucleus (green) moving directly from one human cell into a nearby cell (red).

Using advanced live-cell microscopy, the team observed DNA moving from one cell to another. In one experiment, pieces of the Y chromosome transferred from male cells into female cells. The transferred DNA carried male-specific genes that became active in the female cells, indicating the transferred DNA remained functional after entering the recipient cell.

“There are many open questions. We now want to understand how widespread this process is, how it is regulated at the cellular and molecular levels, and what role it may play in human health and disease, including cancer,” Dr. Ly said. “These findings may have important implications for understanding how cancer genomes evolve and acquire large-scale chromosomal alterations.” 

Researchers also observed DNA transfer between different types of human cells, which Dr. Ly said suggests the findings may be a general feature of human cell biology. 

This research was funded by the National Institutes of Health (NIH), the Cancer Prevention and Research Institute of Texas (CPRIT), the U.S. Department of Defense, The Welch Foundation, a UT Southwestern Haberecht Wildhare-Idea Research Grant, a UT Southwestern Synergy Grant for Collaborative Research, and the Oklahoma Center for Adult Stem Cell Research.

Dr. Ly is a CPRIT Scholar in Cancer Research. Dr. Maurais received an NIH Ruth L. Kirschstein Predoctoral Fellowship from the National Cancer Institute.

About CRI

Children’s Medical Center Research Institute at UT Southwestern (CRI) is a joint venture of UT Southwestern Medical Center and Children’s Medical Center Dallas. CRI’s mission is to perform transformative biomedical research to better understand the biological basis of disease. Located in Dallas, Texas, CRI is home to interdisciplinary groups of scientists and physicians pursuing research at the interface of regenerative medicine, cancer biology, and metabolism – relentless discovery toward the treatments of tomorrow.

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About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – May 14, 2026 – UT Southwestern Medical Center researchers have discovered a key molecular mechanism that allows animals to adapt to changing environmental conditions without altering their genes – an ability known as phenotypic plasticity. The findings, published in Science Signaling, provide a foundation for future studies that could lead to new treatments for a wide range of diseases and disorders, including inflammatory and immune conditions, neurodegenerative diseases, and cancer.

Benjamin Weaver, Ph.D., is Associate Professor of Pharmacology and Physiology and a Virginia Murchison Linthicum Scholar in Medical Research at UT Southwestern.

“This work has just unearthed a vastly underexplored area of basic biology: understanding how changes in the environment can trigger an array of responses within a population of animals. In the future, better understanding of phenotypic plasticity will provide us with a unique opportunity to tune distinct outcomes, leading to healthier responses to stressful environmental conditions,” said study leader Benjamin Weaver, Ph.D., Associate Professor of Pharmacology and Physiology and a Virginia Murchison Linthicum Scholar in Medical Research at UT Southwestern.

The Weaver Lab studies interactions between genes and the environment that affect health. For decades, a key question in this field is how organisms cope with extreme environmental stressors such as excessive heat or cold, heavy exposure to ultraviolet light, or long periods of dehydration or starvation – particularly stressors that individuals have never experienced. Although new genetic variants to help survive challenging conditions can evolve over time, changes to the genome typically take millennia.

“Animals aren’t worried about what will happen 10 million years from now – they’re worried about how to survive in the next five minutes,” Dr. Weaver said. “Yet, how does an animal change its characteristics without changing its genes?”

To answer this question, he and his colleagues focused on a protein called mitogen-activated protein kinase (MAPK) p38. This protein had long been recognized as a stress sensor with diverse roles in development, and it’s found in organisms throughout the animal kingdom as well as in yeast. Previously, it was believed that p38 acted like a switch, turning on or off various molecular pathways in response to changing conditions. But these responses can be opposing even in the same condition, Dr. Weaver explained. For example, p38 appears to promote both cell survival and cell death; in cancer, it can act as both a tumor suppressor and a tumor promoter.

Noted Dr. Weaver: “p38 seems to play both sides of every game.”

To better understand this protein’s role in a live animal, the researchers developed a new analytical method called ContinuumID. It serves as a molecular proximity sensor, allowing researchers to see which proteins come into contact with a selected protein across different tissues, development stages, and environmental conditions.

Dr. Weaver and two of his colleagues – Wang Yuan, Ph.D., Research Scientist and the study's first author, and Yi Weaver, Ph.D., Senior Research Scientist, both in the Weaver Lab – developed this method for use on a p38 family member known as PMK-1 in Caenorhabditis elegans, a roundworm commonly used as a lab model. The researchers found that PMK-1 appeared to interact with more than 1,000 proteins, most of them only under certain circumstances. The connections occurred in different tissues, at different stages of development, and in response to different stressors. When the team examined the known roles of these proteins, most were involved in regulating gene expression.

Additional experiments showed that the same stressor prompted a variety of responses among individual C. elegans worms, even in worms that were genetic clones. These results suggest that PMK-1 doesn’t act as a switch that just turns on and off, but more like a thermostat that can produce a range of outcomes.

This flexibility could help explain why PMK-1 and its counterpart p38 in mammals have been conserved throughout evolution in all animal species, Dr. Weaver said. Although specific outcomes may not benefit every individual, having a range could ensure survival of the population.

The researchers plan to continue studying p38 to better understand how it senses stress and determines which proteins to interact with – knowledge that could help steer its behavior toward healthful responses.

Also contributing to this study was Luke A. Nunamaker, B.S., Research Technician at UT Southwestern.

This study was funded by grants from The Welch Foundation (I-2260-20250403), the National Institute of General Medical Sciences (R35GM133755), and the National Institute on Aging (R21AG086710).

Dr. Weaver is a member of the Cellular Networks in Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center as well as the Hamon Center for Regenerative Science and Medicine at UT Southwestern.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

Benjamin Sabari, Ph.D., is Assistant Professor in the Cecil H. and Ida Green Center for Reproductive Biology Sciences and of Molecular Biology and Obstetrics and Gynecology at UT Southwestern.

The Sabari Lab studies the roles in health and disease of biomolecular condensates, dynamic networks of interacting proteins within cells that help control when genes are turned on and off. In 2023, Dr. Sabari and his colleagues showed that chemical features of some parts of proteins known as intrinsically disordered regions encourage these proteins to join together into biomolecular condensates. A study the team published two years later reported that some fusion proteins – mutant proteins caused by the melding of two genes – drive select cancers by confining an enzyme called RNA polymerase II within biomolecular condensates.

Discovering ways to inhibit this process could lead to new treatments for some cancers by allowing researchers to control the behavior of specific oncogenes, genes that encourage the development and spread of cancer, Dr. Sabari explained.

“The Pershing Square Sohn Cancer Prize will empower my lab to pursue a high-risk, high-reward direction that existing funding mechanisms are not designed to support: developing new strategies to target the unique multivalent molecular organization of oncogenic transcription rather than generally inhibiting transcription,” he said. “If successful, this work will establish a new paradigm for treating cancers driven by dysregulation of gene transcription.”

Dr. Sabari joined the faculty at UT Southwestern in 2020. He was a Damon Runyon Postdoctoral Fellow at the Whitehead Institute. He earned his bachelor’s degree in molecular genetics from the University of Rochester and his doctoral degree at The Rockefeller University as a National Science Foundation Graduate Research Fellow. He is a member of the Cellular Networks in Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

The Pershing Square Sohn Cancer Prize is funded by the Pershing Square Sohn Cancer Research Alliance, formed in 2013 by The Pershing Square Foundation. The Alliance is dedicated to accelerating cures for cancer by supporting innovative cancer research and facilitating collaborations between academia and industry. Previously awarded only to cancer research scientists and physician-scientists based in the greater New York City area, the Prize became open to scientists across the U.S. this year.

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – May 01, 2026 – Loss of an enzyme necessary for a process called lipoylation disrupts the way cancer cells copy their DNA, increasing their vulnerability to a class of anticancer drugs known as PARP inhibitors, a study led by UT Southwestern Medical Center researchers shows. The findings, published in Science Advances, reveal a previously unrecognized mechanism to protect DNA replication and genome stability that could lead to new treatments for some cancers.  

Yuanyuan “Faith” Zhang, M.D., Ph.D., is Assistant Professor of Radiation Oncology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

“This study shows that metabolism doesn’t just fuel cancer cells – it also directly shapes how DNA is copied and protected. This helps explain why inhibiting lipoylation could make tumors especially sensitive to PARP inhibitors,” said Yuanyuan “Faith” Zhang, M.D., Ph.D., Assistant Professor of Radiation Oncology and a member of the Experimental Therapeutics Research Program in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. Dr. Zhang co-led the study with first author Zengfu Shang, Ph.D., Assistant Professor of Radiation Oncology in the Zhang Lab.

Lipoylation is a process in which an enzyme called LIPT1 adds lipoic acid to other enzymes in the energy-producing organelles known as mitochondria. In 2025, Dr. Zhang, Dr. Shang, and their colleagues showed that blocking lipoylation with a drug called CPI-613 enhanced the effect of radiation in preclinical models of lung cancer. That study showed that this effect stemmed from problems in DNA damage repair.

To better understand this phenomenon, researchers used gene editing to delete the LIPT1-producing gene in three different cell lines. Each altered cell line multiplied significantly slower and formed fewer colonies than unaltered cells. Further investigation suggested that this behavior was due to replication stress, an impaired ability of cells to copy their DNA in preparation for cell division.

Further experiments showed that deleting LIPT1 led to an accumulation of the metabolite 2-hydroxyglutarate, which caused DNA to become tightly compacted in cell nuclei. In turn, this slowed new DNA synthesis at replication forks, structures in which double strands of DNA separate to begin the copying process. The cells’ attempt to restart the stalled replication fork subsequently prompted the formation of single-strand DNA breaks that necessitated repair with another protein known as poly (ADP-ribose) polymerase 1, or PARP1.

Zengfu Shang, Ph.D., is Assistant Professor of Radiation Oncology at UT Southwestern.

PARP1 is a known target for PARP inhibitors, a class of cancer-fighting drugs, Dr. Shang explained. When the team treated cells missing LIPT1 with a PARP inhibitor, the cancer cells couldn’t repair their damaged DNA, a deficit that proved lethal.

Drs. Zhang and Shang said that low levels of LIPT1, frequently present in some cancer types, could potentially serve as a biomarker for sensitivity to PARP inhibitors. Similarly, combining CPI-613 – a lipoylation inhibitor designated as an orphan drug by the Food and Drug Administration with well-documented safety data in cancer patients – with PARP inhibitors could offer a new strategy for treating non-small cell lung cancers and other cancer types with low LIPT1. The team plans to investigate both possibilities in future studies.

Other UTSW researchers who contributed to this study are Anthony J. Davis, Ph.D., Associate Professor of Radiation Oncology; Ching-Cheng Hsu, Ph.D., Research Associate; Jui-Chung Chiang, Ph.D., postdoctoral fellow; and Ciara Newman, B.S., a former research assistant who is now a graduate student researcher.

This study was funded by a Lung SPORE Career Enhancement Award; a Distinguished Researcher Award from the President’s Research Council; an Institutional Research Grant from the American Cancer Society (IRG-21-142-16); a National Cancer Institute (NCI) Cancer Center Support Grant (P30CA142543); awards from the National Center for Advancing Translational Sciences of the National Institutes of Health (KL2TR003981 and CTSA-PP-YR1-D-009); a Startup Award from UT Southwestern Department of Radiation Oncology; a Disease-Oriented Clinical Scholar Award from UT Southwestern; and grants from the National Institutes of Health (R01CA276058 and R01CA29290), the Department of Energy (DE-SC0025578), and the National Aeronautics and Space Administration (20-20HHCSR_2-0033).

About UT Southwestern Medical Center

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 27 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

Intervention to promote hydration fails to reduce kidney stone recurrence

About 1 in 11 people in the U.S. experience urinary stone disease – more commonly known as kidney stones – according to the National Institute of Diabetes and Digestive and Kidney Diseases. Increasing fluid intake has long been recommended to decrease the risk of recurrence in those who develop this painful condition. However, studies have shown that maintaining high fluid intake can be difficult.

A nationwide team of researchers including Naim Maalouf, M.D., Professor of Internal Medicine and Associate Director of the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research at UT Southwestern Medical Center, conducted the Prevention of Urinary Stones with Hydration (PUSH) clinical trial at six U.S. academic medical centers between 2017 and 2024 to test whether a behavioral intervention could increase fluid intake over two years. In Dallas, participants were recruited from UTSW, Parkland Health, and Children’s Health.

The researchers divided 1,658 adolescents and adults who had experienced a kidney stone within the past three years into two groups, with each given recommendations to increase urine output to at least 10.5 cups per day. To achieve this goal, one group received a personalized “fluid prescription”; a Bluetooth-enabled “smart” water bottle; a financial incentive to meet daily water intake; health coaching to troubleshoot fluid intake barriers; and additional help of their choice, including encouraging text messages or a support partner. The other group received the smart water bottle and general instructions for stone prevention, but no other assistance.

Results published in The Lancet showed the group that received the multifaceted intervention had slightly more urine output than the other group. However, the rates of kidney stone recurrence were approximately the same between the two groups. Further research is needed to find more innovative ways to increase water consumption to levels that effectively prevent kidney stone formation, and to identify alternative strategies for stone prevention including diet and/or medications, the study authors said.

Many older adults diagnosed with cancer in the emergency department

More than 1 in 3 older U.S. adults with common cancers are diagnosed during an emergency department (ED) visit – a pathway linked to poorer outcomes and gaps in routine care, according to a study published in JNCI Cancer Spectrum. The study analyzed Surveillance, Epidemiology, and End Results (SEER)‑Medicare data from over 600,000 patients 66 and older who were diagnosed with 14 cancer types between 2008 and 2017.

Most emergency diagnoses resulted in hospitalization, according to the data. However, a notable subgroup – those diagnosed in the ED who were not admitted – were more likely to live in rural areas and have earlier-stage disease. Compared with patients diagnosed in nonemergency situations, those with emergency diagnoses had more prior emergency room visits and less outpatient care for possible cancer symptoms.

The findings suggest that some emergency diagnoses reflect missed opportunities for timely detection and access to routine care. Identifying and reducing avoidable barriers could improve cancer outcomes and inform health care quality metrics.

Contributing to the study were Sandi Pruitt, Ph.D., Professor, and Megan Mullins, Ph.D., Assistant Professor, both in the Peter O’Donnell Jr. School of Public Health at UT Southwestern. Drs. Pruitt and Mullins are members of the Harold C. Simmons Comprehensive Cancer Center.

Children on life support show biological signs of brain injury

A study published in JAMA Pediatrics found that critically ill children receiving extracorporeal membrane oxygenation (ECMO) often show biological signs of brain injury that may not be detected through routine clinical assessments. The multicenter study measured blood-based biomarkers associated with brain injury in 219 children treated with ECMO between 2019 and 2023 and examined how those markers related to neurologic outcomes and survival.

Researchers found that several plasma biomarkers were elevated during ECMO support and were associated with acute brain injury and poorer clinical outcomes. Levels of these biomarkers changed over time, suggesting ongoing neurologic risk during treatment.

The findings signal that blood-based biomarkers could help clinicians identify brain injury earlier, monitor neurologic risk during ECMO, and potentially guide strategies to protect the developing brain in critically ill children.

Michael Bell, M.D., Professor of Pediatrics and Chief of the Division of Pediatric Critical Care at UT Southwestern, contributed to this study.

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 24 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of nearly 3,400 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

About Parkland Health

Parkland Health is one of the largest public hospital systems in the country. Premier services at the state-of-the-art Parkland Memorial Hospital include the Level I Rees-Jones Trauma Center, the only burn center in North Texas verified by the American Burn Association for adult and pediatric patients, and a Level III Neonatal Intensive Care Unit. The system also includes two on-campus outpatient clinics – the Ron J. Anderson, MD Clinic and the Moody Outpatient Center, as well as more than 30 community-based clinics and numerous outreach and education programs. By cultivating its diversity, inclusion, and health equity efforts, Parkland enriches the health and wellness of the communities it serves. For more information, visit parklandhealth.org.

DALLAS – April 14, 2026 – Zhijian “James” Chen, Ph.D., Professor of Molecular Biology at UT Southwestern Medical Center and one of the world’s top researchers on how the body’s immune system protects against threats such as bacteria and viruses, has been awarded the 2026 Japan Prize in Life Sciences – one of the highest international honors for science and technology.

The award recognizes Dr. Chen’s discoveries related to the innate immune system including cyclic GMP-AMP synthase, or cGAS, which acts as the body’s burglar alarm to trigger defense from invading pathogens. Dr. Chen shares this year’s Japan Prize with Shizuo Akira, M.D., Ph.D., Professor at Osaka University.

Zhijian "James" Chen, Ph.D., is Professor of Molecular Biology and Director of the Center for Inflammation Research at UT Southwestern Medical Center. He holds the George L. MacGregor Distinguished Chair in Biomedical Science.

“I am extremely honored and humbled to be selected to receive the Japan Prize,” said Dr. Chen, who is a Howard Hughes Medical Institute Investigator and Director of the Center for Inflammation Research at UT Southwestern. “This recognition validates the collaborative work of scientists at UT Southwestern and worldwide to expand our understanding of human disease. I am grateful to the students, postdoctoral fellows, and staff members in my lab for their hard work and to the leadership at UT Southwestern for their unwavering support.”

“Dr. Chen’s breakthroughs have significantly advanced the field of immunology, paving the way for new approaches to the development of more effective vaccines and novel therapies for a broad range of diseases, including cancer and autoimmune disorders,” said Daniel K. Podolsky, M.D., President of UT Southwestern. “The entire UT Southwestern community takes great pride in seeing the impact of Dr. Chen’s work recognized by this very special high honor.”

The Japan Prize was presented in Tokyo on April 14, during Japan Prize Week, which included award ceremonies attended by the Emperor and Empress of Japan and commemorative lectures by the laureates.

Established in 1983, the Japan Prize is awarded annually to scientists and researchers from around the world, recognizing individuals who have contributed significantly to peace and prosperity through original and outstanding achievements that have greatly advanced the progress of science and technology.

Dr. Chen’s discoveries have elucidated the process by which the human body fights off invasive viruses, bacteria, and other microbes. In 2012, his laboratory identified cGAS, which triggers the innate immune system when it detects foreign DNA inside a cell. Earlier, he identified the first mitochondrial protein known to be involved in immunity against infections, which he dubbed MAVS, describing its function (mitochondrial antiviral signaling) and honoring his favorite basketball team, the Dallas Mavericks.

His research has been recognized with some of the most esteemed awards in science, including the Paul Ehrlich and Ludwig Darmstaedter Prize (2025), the Albert Lasker Basic Medical Research Award (2024), the Louisa Gross Horwitz Prize (2023), and the Breakthrough Prize in Life Sciences (2019), among others.

Dr. Chen is a member of both the National Academy of Sciences and the National Academy of Medicine and a Fellow of the Royal Society of the United Kingdom. At UTSW, he is a member of the Center for the Genetics of Host Defense as well as the Harold C. Simmons Comprehensive Cancer Center. He holds the George L. MacGregor Distinguished Chair in Biomedical Science.

DALLAS – Jan. 12, 2026 – UT Southwestern Medical Center has received an award from the Advanced Research Projects Agency for Health (ARPA-H) to develop livers using patients’ own cells and an innovative three-dimensional (3D) printing approach. If successful, this project – known as Vascularized Immunocompetent Tissue as an Alternative Liver (VITAL) – could significantly reduce the gap between supply and demand for donor livers, negate the necessity of lifelong immunosuppression for liver transplant patients, and create artificial livers for in vitro drug testing and research. The project is under ARPA-H’s Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, which is led by ARPA-H Program Manager Ryan Spitler, Ph.D.

Muhammad Rizwan, Ph.D., Assistant Professor of Biomedical Engineering and Ophthalmology at UT Southwestern, is the project’s principal investigator.

“Over the last two decades, researchers have made remarkable progress toward the goal of creating lab-made organs, including innovations in biomaterials, stem cell differentiation, and bioprinting. UT Southwestern is an ideal environment to bring together the recent advances that have never been combined before,” said the project’s principal investigator, Muhammad Rizwan, Ph.D., Assistant Professor of Biomedical Engineering and Ophthalmology at UT Southwestern.

Each year, liver cirrhosis and chronic liver diseases cause about 50,000 deaths in the U.S. As of September 2024, nearly 10,000 people were on the waiting list for a donor liver, with wait times averaging about seven months, according to the Health Resources & Services Administration. Statistics show that up to 31% of patients die while waiting for a donor liver.

Researchers have attempted to narrow the gap between donor liver supply and demand in many ways, such as pursuing living donors or improving technology that keeps cadaver donor livers healthy for a longer time before transplant, said Madhukar Patel, M.D., M.B.A., Sc.M., Assistant Professor of Surgery at UTSW, Surgical Director of the Liver Transplantation Program, and a Dedman Family Scholar in Clinical Care. However, none of these approaches has significantly resolved the lack of sufficient donor livers. Finding a way to generate artificial livers that function as well as natural ones could offer a solution, he explained. Artificial livers may also address other issues inherent to organ transplants, such as the need for lifelong immunosuppression and the high cost of liver transplantation, which averages nearly $1 million.

Madhukar Patel, M.D., M.B.A., Sc.M., is Assistant Professor of Surgery at UT Southwestern, Surgical Director of the Liver Transplantation Program, and a Dedman Family Scholar in Clinical Care.

Toward that goal, ARPA-H recently awarded UTSW up to $25 million for VITAL. In this project, researchers across UTSW, including Drs. Rizwan and Patel, will work together to harvest cells from liver disease patients and facilitate their conversion into induced pluripotent stem cells (iPSCs), which can become any cell type in the body. Jun Wu, Ph.D., Associate Professor of Molecular Biology, whose lab specializes in working with iPSCs, will lead research to reprogram the patient cells into iPSCs and convert these cells into the various cell types that make up livers. The team will then combine these cells with a hydrogel “bioink” that can be used for 3D printing of functioning livers. These bioprinted livers will first be tested in small and large animal models and potentially within humans in about five years, Dr. Rizwan said. Collaborators from Pennsylvania State University, led by Ibrahim T. Ozbolat, and the University of California, Davis, will assist with improving the 3D printing technology and GMP cell manufacturing.

Researchers at UTSW and elsewhere have successfully created liver tissue by converting iPSCs to liver cells. However, Dr. Rizwan said, a major roadblock to scaling this tissue into an artificial liver is the lack of blood vessels and bile ducts, tubes that remove bile acids that build up from normal liver function. He and his colleagues have discovered a novel approach for growing both blood vessels and bile ducts within generated liver tissue, making it possible to create a fully functional artificial liver. Moreover, Dr. Rizwan is establishing a scalable organoid manufacturing facility at UT Southwestern.

Because the resulting organ will be custom-made from a patient’s own cells, he added, transplanted livers won’t require immunosuppression. In addition, he estimates a bioprinted liver could be generated in 10-13 weeks. These artificial organs won’t just be useful for transplantation, Dr. Rizwan explained. The process of developing livers from scratch is expected to lend insight into how natural livers function, helping researchers solve long-standing mysteries about this organ. Artificial livers will also be used to evaluate the safety and efficacy of pharmaceuticals in development.

Samuel Achilefu, Ph.D., is inaugural Chair of Biomedical Engineering and Professor in the Harold C. Simmons Comprehensive Cancer Center and of Radiology at UT Southwestern and a co-investigator on this project.

The wealth of expertise and collaboration available at UTSW makes it an ideal location for developing artificial livers, said Samuel Achilefu, Ph.D., inaugural Chair of Biomedical Engineering and Professor in the Harold C. Simmons Comprehensive Cancer Center and of Radiology at UTSW. A co-investigator on this project, he will use his expertise in noninvasive imaging to evaluate the performance of the bioprinted livers.

UTSW has a robust solid organ transplant program that recently celebrated its 1,000th liver transplant and houses experts across the spectrum needed for developing artificial livers. In addition, the seven UTSW researchers leading portions of this project, the 11 core facilities they will use, and UTSW’s hepatology clinics are all within walking distance, facilitating teamwork.

“This project represents a bold step toward advancing patient care through biomedical innovation,” Dr. Achilefu said. “It unites engineers, clinicians, and scientists to transform discovery into real-world solutions, shaping a future where functional organ printing becomes reality.”

Other UTSW co-investigators involved in the project are Hao Zhu, M.D., Professor of Children’s Medical Center Research Institute at UT Southwestern; Walter Akers, Ph.D., D.V.M., Associate Professor of Biomedical Engineering; and Yasin Dhaher, Ph.D., Professor of Physical Medicine & Rehabilitation.

Dr. Wu is a Virginia Murchison Linthicum Scholar in Medical Research. Dr. Achilefu holds the Lyda Hill Distinguished University Chair in Biomedical Engineering. Dr. Zhu holds the Nancy B. and Jake L. Hamon Distinguished Chair in Therapeutic Oncology Research. Drs. Achilefu, Akers, Rizwan, Wu, and Zhu are members of the Simmons Cancer Center.

This publication was supported by the Advanced Research Projects Agency for Health (ARPA-H) under Award Number D25AC000239-00, providing up to $24,939,120 for a 60-month period. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Advanced Research Projects Agency for Health.

DALLAS – March 25, 2026 – UT Southwestern Medical Center researchers have identified how the quintessential immune protein known as stimulator of interferon genes (STING) migrates from one cellular organelle to another, a necessary step in its activation. The findings, reported in Cell, could eventually lead to new therapeutics that harness this system to fight infections, cancer, autoimmune disorders, and neurodegenerative diseases.

“Our study revealed structural insight on how STING achieves a controlled exit from the endoplasmic reticulum, which is essential for a balanced immune response,” said Nan Yan, Ph.D., Vice Chair and Professor of Immunology and Professor of Microbiology at UT Southwestern. Dr. Yan co-led the study with first author Heng Lyu, Ph.D., a postdoctoral researcher in the Yan Lab.

Nan Yan, Ph.D., is Vice Chair and Professor of Immunology and Professor of Microbiology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He holds the Edwin L. Cox Distinguished Chair in Immunology and Genetics and is a Rita C. and William P. Clements, Jr. Scholar in Medical Research.

STING is a key part of the innate immune system, which provides broad and early protection against foreign invaders – such as viruses, bacteria, fungi, and parasites – as well as cancer. One trigger for innate immunity is DNA in the cytoplasm of cells. A protein called cGAS, discovered in 2012 by Zhijian “James” Chen, Ph.D., Professor of Molecular Biology and Director of the Center for Inflammation Research at UT Southwestern, senses this DNA. In response, it produces a molecule called cGAMP that binds to STING, which resides in a cellular organelle called the endoplasmic reticulum (ER) when it’s inactive.

After cGAMP binding, STING molecules are turned on, linking in a string (a process called oligomerization) and migrating to an organelle called the Golgi – a process the Yan Lab discovered in 2015. There, they activate additional molecules in a signaling cascade that prompts immune activity. STING’s oligomerization is necessary for this to occur.

Recent research led by Dr. Chen and colleagues, reported in two papers published concurrently in Nature, provided mechanistic and structural insight into how STING oligomerizes and why it needs to move from the ER to the Golgi. But how STING makes this migration and why oligomerization is critical to this process has been unclear.

To answer these questions, Dr. Yan and his team genetically engineered cells to delete four proteins that belong to a group called SEC24, which ferries proteins from the ER to other cellular locations. In those missing the protein known as SEC24C, STING could no longer initiate its immune signaling cascade when stimulated with a synthetic analog of cGAMP. These results suggest SEC24C moves STING from the ER to the Golgi.

Heng Lyu, Ph.D., is a postdoctoral researcher in the Yan Lab at UT Southwestern.

To further confirm the interaction between these two proteins, the researchers used AlphaFold3 – a powerful artificial intelligence program that predicts the shape of proteins from their genetic sequence. They wanted to determine how SEC24C might bind to a pair of STING molecules attached together, the state in which STING exists in the ER. Their findings showed SEC24C appears to bind to STING in a region without a defined structure.

When the researchers mutated this region on STING, it no longer left the ER to migrate to the Golgi. The team had similar results when it mutated the region on SEC24C that AlphaFold3 predicted would bind to STING. These results suggested the disordered region on STING binds to a corresponding region on SEC24C to exit the ER.

Similarly, preventing STING from oligomerizing also stopped it from leaving the ER. A closer look showed that, unlike other proteins that SEC24C ferries from the ER to other cellular locations, STING’s disordered region is too short to bind strongly to the corresponding region on SEC24C. Thus, oligomerization is critical for creating a longer molecule that binds more strongly to SEC24C. This imperfect binding could be a way for cells to limit how easily STING is activated, Dr. Yan explained – an important protection against chronic STING activation that causes autoimmune disorders.

Further experiments showed that mutating the disordered region so it couldn’t bind to SEC24C impaired STING’s ability to fight off viral infections in cells. Conversely, mutations that increased binding strength to SEC24C boosted STING activity, helping it fight tumors in an animal cancer model.

Using drugs to tinker with STING’s binding to SEC24C could represent a new strategy for decreasing STING’s activity, possibly leading to treatments for autoimmune or neurodegenerative conditions, or for increasing it, potentially fighting infections or cancer. Dr. Yan and his colleagues plan to continue research toward this goal.

Other UTSW researchers who contributed to this study are Xuewu Zhang, Ph.D., Professor of Pharmacology and Biophysics; Wanwan Huai, Ph.D., Kun Song, Ph.D., and Hui Zhang, Ph.D., postdoctoral researchers; and Cong Xing, B.S., graduate student researcher.

Dr. Yan holds the Edwin L. Cox Distinguished Chair in Immunology and Genetics and is a Rita C. and William P. Clements, Jr. Scholar in Medical Research. Dr. Chen holds the George L. MacGregor Distinguished Chair in Biomedical Science. Drs. Yan and Chen are members of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

This study was funded by grants from the National Institutes of Health (AI151708 and R01CA273595), the Cancer Prevention and Research Institute of Texas (RP220242), and The Welch Foundation (I-1702).

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 24 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 3,300 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

The partnership centers on InterAct’s proprietary computational engine, which “cracks the biological code” of how cancer spreads, according to the company. The lead asset, IAT-S2, is a validated AAV8-based gene therapy specifically engineered to treat breast cancer liver metastasis (BCLM), a condition with historically limited treatment options and high mortality rates.

Daniel Hommes, M.D., Ph.D., is Vice President and Chief Innovation Officer at UT Southwestern.

“The UTSW Innovation Hub is dedicated to ensuring that our most promising scientific discoveries reach the patients who need them most,” said Daniel Hommes, M.D., Ph.D., Vice President and Chief Innovation Officer at UT Southwestern. “InterAct’s unique computational approach to metastasis, combined with our foundational research, creates a powerful synergy. We are proud to partner with a team that has shown such rapid clinical and operational progress.”

Isaac Chan, M.D., Ph.D., is Assistant Professor of Internal Medicine in the Division of Hematology and Oncology and of Molecular Biology at UT Southwestern. Dr. Chan is a member of the Harold C. Simmons Comprehensive Cancer Center at UTSW.

The agreement capitalizes on the cancer research of Isaac Chan, M.D., Ph.D., Assistant Professor of Internal Medicine in the Division of Hematology and Oncology and of Molecular Biology at UT Southwestern. Dr. Chan is a member of the Cellular Networks in Cancer Research Program in the Harold C. Simmons Comprehensive Cancer Center at UTSW.

InterAct’s momentum accelerated significantly in early 2026. The company was recently selected for the Charles River Incubator Program, a prestigious endorsement that provides the dedicated manufacturing scale necessary to advance IAT-S2 and InterAct’s broader pipeline toward clinical trials.

“This licensing agreement is a pivotal milestone for InterAct,” said Dan Hargrove, CEO of InterAct Therapeutics. “InterAct is at the forefront of cracking the biological code of how invasive cancer cells displace healthy host cells. By leveraging the pioneering work of Dr. Isaac Chan and the Chan Lab at UT Southwestern, we have developed a way to reverse this process. Yet our approach doesn’t just turn the host environment into a barrier against disease; it trains healthy host cells to become cancer killers.

Dan Hargrove is CEO of InterAct Therapeutics.

“We are deeply grateful to UT Southwestern, a powerhouse in cancer research, for its partnership in this mission and the significant support of the UTSW Innovation Hub. Following productive discussions with the Food and Drug Administration and our selection into the Charles River Incubator Program, we are moving with urgency toward clinical trials for our lead breast cancer liver metastasis indication, targeting a major unmet need with a first-in-class therapy.”

InterAct will present further details on its progress and the IAT-S2 program at the Charles River Laboratories (CRL) Cell & Gene Therapy Summit on March 25-26 in Cambridge, Massachusetts.

Dr. Chan is a co-founder and Chief Scientific Officer of InterAct Therapeutics.

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 24 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 3,300 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

About InterAct Therapeutics Inc.

InterAct is a biotechnology company dedicated to treating cancer metastasis at its source. Through our proprietary InterAct Print™ platform, we identify the biological drivers of infiltration and engineer therapies to reprogram the host environment into a barrier against metastatic cancers while training host cells to become cancer killers. Our lead program, IAT-S2, is a first-in-class AAV8 gene therapy for breast cancer liver metastasis (BCLM). Beyond the liver, the InterAct Print™ framework is designed to target the most common metastatic sites, including the lung and brain, utilizing a diverse toolkit of AAV, mRNA, and siRNA modalities.

DALLAS – March 20, 2026 – On Friday morning, UT Southwestern Medical School’s Class of 2026 crowded inside the Bryan Williams, M.D. Student Center gymnasium for the time-honored tradition of National Match Day. At precisely 11 a.m., the soon-to-be graduates – along with thousands of other medical students nationwide – tore open the envelopes revealing where they will begin the next phase of their training as resident physicians.

In total, 239 UT Southwestern students matched with more than 80 residency programs across the U.S. Cheers erupted as the aspiring doctors discovered they would be heading to prestigious medical centers such as those at Duke, Johns Hopkins, and Stanford universities after graduating in May. Eighty-one students will continue their training at UTSW-affiliated programs, which rank among the top in the country.

U.S. News & World Report named UT Southwestern among its Best Medical Schools for 2024-2025 – Tier 1 (top 16) for research and Tier 2 (top 50) for primary care. UTSW has the largest graduate medical education training program in Texas, with more than 1,400 clinical residents completing their medical education with postgraduate specialty and subspecialty training.

“Match Day is a momentous milestone in every physician’s journey, and as an educator, it is immensely gratifying to stand beside our students as they prepare to take the next step toward their future,” said Angela Mihalic, M.D., Dean of Medical Students and Associate Dean for Student Affairs at UT Southwestern Medical School, Professor of Pediatrics, and a Distinguished Teaching Professor.

“We are confident that the time and effort they have invested here will lead them to achieve great things in this next phase of their medical training,” she said. “To answer the call of this vocation is no small thing, and I see the boundless potential in each and every one of these future physicians. I have no doubt that the values instilled in them at UT Southwestern will serve as a guiding light to treat their patients with competence and compassion.”

This year, the National Resident Matching Program matched more than 41,000 medical students to institutions across the country. Top specialty selections for UT Southwestern students include Internal Medicine, Pediatrics, and Psychiatry.

“Growing up in East Texas, I viewed UT Southwestern as the pinnacle of cutting-edge medicine, a perception that was reinforced throughout my undergraduate education,” said Michael Pitonak, who hails from Tyler and will train in internal medicine at Duke University Medical Center in North Carolina. “During that time, I came to understand why UT Southwestern holds this reputation.”

Today, this reflection is echoed by many others in the graduating class.

“I was first exposed to medicine through my dad, a physician, as I watched him save lives,” said Zuhair Hawa, who will train in neurosurgery at University of Pittsburgh Medical Center in Pennsylvania. “After gaining more experience at UT Southwestern, I discovered a deep appreciation for the direct interactions we have with patients each day. I enjoy learning their stories and making all patients feel safe and heard during their most vulnerable moments. As a physician, I aspire to comfort patients through these experiences and guide them toward healing.”

UTSW training opportunities, rankings, distinctions

UT Southwestern’s training facilities include William P. Clements Jr. University Hospital, ranked by U.S. News & World Report as the No. 1 hospital in Dallas-Fort Worth for nine consecutive years; Parkland Memorial Hospital, one of the nation’s busiest public hospitals; and Children’s Medical Center Dallas, one of the largest children’s hospitals in the country and the only hospital in North Texas to be ranked in all pediatric specialties in U.S. News’ annual Best Children’s Hospitals report. UT Southwestern also houses a 49,000-square-foot Simulation Center – one of the largest of its kind.

UT Southwestern is nationally ranked by U.S. News in 12 specialties, the most of any in Texas: Cancer; Cardiology, Heart, and Vascular Surgery; Diabetes and Endocrinology; Ear, Nose, and Throat; Gastroenterology and Gastrointestinal Surgery; Geriatrics; Neurology and Neurosurgery; Obstetrics and Gynecology; Orthopedics; Pulmonology and Lung Surgery; Rehabilitation; and Urology. It is also rated “High Performing” in the great majority of evaluated conditions and procedures, from aortic valve surgery and hip fracture to back surgery (spinal fusion) and stroke care.

Other key distinctions

• UTSW’s Harold C. Simmons Comprehensive Cancer Center is the first and only National Cancer Institute-designated comprehensive cancer center in North Texas – one of only 57 across the U.S.
• UTSW is designated as an Advanced Comprehensive Stroke Center by The Joint Commission and the American Heart Association/American Stroke Association and has a Level 4 Epilepsy Center, the highest possible rating awarded by the National Association of Epilepsy Centers.
• UTSW scientists currently lead more than 6,200 research projects, supported by more than $816 million in funding.
• The Perot Family Scholars Medical Scientist Training Program, one of only 56 M.D./Ph.D. training programs in the country supported by the National Institutes of Health (NIH), offers a dual degree to strengthen the advancement of laboratory discoveries into the clinical arena.
• UTSW is ranked No. 1 globally among health care institutions by Nature Index for publishing high-quality scientific research.
• UTSW was awarded Press Ganey’s 2025 Guardian of Excellence Award, which recognizes the top 5% of health care organizations in delivering patient experience.

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 24 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 3,300 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – March 19, 2026 – A widely used fracture risk calculator may help guide surgical decisions to treat patients with an endocrine disorder called primary hyperparathyroidism (PHPT) that causes progressive bone loss, according to a study led by UT Southwestern Medical Center researchers. The findings, published in JAMA Network Open, suggest the Fracture Risk Assessment Tool (FRAX) could be used to identify patients who may benefit from a parathyroidectomy to potentially prevent fractures.

“The study provides the first large-scale validation of FRAX in primary hyperparathyroidism and reframes fracture prevention as a quantifiable, risk-based outcome for surgical decision-making rather than relying solely on bone density thresholds,” said lead author Vivek Sant, M.D., Assistant Professor of Surgery at UT Southwestern.

Vivek Sant, M.D., is Assistant Professor of Surgery at UT Southwestern.

PHPT affects nearly 3 million Americans and occurs when the parathyroid glands produce an excess amount of hormones, raising blood calcium levels and weakening bones over time. The condition can increase the risk of fragility fractures, particularly in older adults and postmenopausal women. Although parathyroidectomy – surgery to remove the overactive parathyroid gland or glands – is the only curative treatment, determining who should undergo the procedure can be challenging. 

To investigate whether FRAX could help guide treatment decisions, UTSW researchers identified 59,194 adults ages 40 to 90 from a national database who were diagnosed with PHPT between 2000 and 2024. About one-quarter of patients underwent parathyroidectomy, while the remainder were treated without surgery.

In a retrospective analysis of the data, FRAX assigned a score to predict a patient’s risk of fractures. Researchers found FRAX performed reasonably well in identifying which patients with PHPT would benefit from parathyroidectomy, even when bone mineral density data were not available. Compared with nonsurgical management, parathyroidectomy was associated with lower fracture risk when patients’ FRAX scores reached relatively modest levels. 

Naim Maalouf, M.D., is Professor of Internal Medicine and Associate Director of the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research at UT Southwestern. He holds The Frederic C. Bartter Professorship in Vitamin D Research and is a member of the Harold C. Simmons Comprehensive Cancer Center.

The analysis also found that many patients who do not meet current guideline-based criteria for surgery may still exceed these risk thresholds. Among patients who did not meet traditional surgical criteria, 25% had FRAX hip fracture scores above the level associated with fracture reduction after surgery.

“These findings give clinicians a practical, widely available tool to personalize discussions about surgery, enabling more informed shared decision-making,” said senior author Naim Maalouf, M.D., Professor of Internal Medicine and Associate Director of the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research at UT Southwestern.

The study builds on previous work at UTSW examining fracture outcomes in patients with PHPT and adds new evidence supporting risk-based approaches to surgical care.

Other UTSW researchers who contributed to this study are Yaser ElNakieb, Ph.D., Senior Data Scientist; Justin Rousseau, M.D., M.M.Sc., Associate Professor of Neurology and in the Peter O’Donnell Jr. Brain Institute and Deputy Chief Medical Informatics Officer for Neurosciences; Yu-Lun Liu, Ph.D., Associate Professor in the Peter O’Donnell Jr. School of Public Health; and Craig Rubin, M.D., Professor Emeritus of Internal Medicine. 

Dr. Maalouf holds The Frederic C. Bartter Professorship in Vitamin D Research. He is a member of the Harold C. Simmons Comprehensive Cancer Center.

The study was supported by the American Association of Endocrine Surgeons Foundation Paul LoGerfo Research Award and the National Center for Advancing Translational Sciences of the National Institutes of Health.

About UT Southwestern Medical Center 

UT Southwestern, one of the nation’s premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty members have received six Nobel Prizes and include 24 members of the National Academy of Sciences, 25 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 3,300 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians in more than 80 specialties care for more than 143,000 hospitalized patients, attend to more than 470,000 emergency room cases, and oversee nearly 5.3 million outpatient visits a year.

DALLAS – March 11, 2026 – A growing number of U.S. adults consider electronic cigarettes (e-cigarettes) more harmful than conventional cigarettes, UT Southwestern Medical Center researchers show in a study. The findings, published in Nicotine and Tobacco Research, could have significant implications for public health policymakers, tobacco control strategies, and people who use either of these cigarette types.

David Gerber, M.D., is Professor of Internal Medicine and in the Peter O’Donnell Jr. School of Public Health and Co-Director of the Office of Education and Training in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

“The perception that e-cigarettes are more harmful than cigarettes has been linked to both a decreased willingness to use e-cigarettes for smoking cessation and an increased likelihood of switching from vaping to smoking. Understanding the ramifications of this perception change represents a critical consideration when developing cessation strategies,” said David Gerber, M.D., Professor of Internal Medicine and in the Peter O’Donnell Jr. School of Public Health and Co-Director of the Office of Education and Training in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

Dr. Gerber co-led the study with Cristina Thomas, M.D., Assistant Professor of Dermatology and Internal Medicine, and Alexander Wu, B.S., a medical student at UTSW and the study’s first author.

Cigarette smoking has declined significantly over the past few decades, from a historical peak in 1965 when 43% of U.S. adults reported smoking to about 12% in 2025, according to the Centers for Disease Control and Prevention. However, since e-cigarettes, or “vapes,” were introduced in the U.S. in 2006, their use has steadily grown: Nearly 7% of U.S. adults reported using these devices in 2025.

Cristina Thomas, M.D., is Assistant Professor of Dermatology and Internal Medicine at UT Southwestern.

According to physicians, e-cigarettes are generally thought to be less harmful than conventional cigarettes, which are known to cause cardiovascular disease, pulmonary disease, and several forms of cancer, Dr. Thomas explained. However, a growing awareness of e-cigarettes’ hazards – including exposure to high levels of addictive nicotine and toxic chemicals as well as a propensity to act as a gateway for conventional cigarette smoking – led the Food and Drug Administration to include e-cigarettes in its 2018 anti-smoking campaign aimed at youth called “The Real Cost.” A year later, an outbreak of e-cigarette or vaping product use-associated lung injury (EVALI) occurred, affecting the health of thousands of e-cigarette users.

To learn how these events may have affected public perception of e-cigarettes, Mr. Wu and his colleagues analyzed data from the Health Information Nation Trends Survey (HINTS) from 2012 to 2022. This cross-sectional, nationally representative survey sponsored by the National Cancer Institute collects a variety of health data each year.

Alexander Wu, B.S., is a medical student at UT Southwestern and the study’s first author.

Using answers from 20,771 survey respondents, the researchers found that the proportion perceiving e-cigarettes as more harmful than conventional cigarettes rose from nearly 3% in 2012 to more than 30% in 2022. Similarly, perceptions of e-cigarettes as less harmful decreased from nearly 51% in 2012 to about 17% in 2022. An analysis of data collected before and after “The Real Cost” campaign and the EVALI outbreak suggests that these events negatively affected public perceptions of e-cigarettes, Mr. Wu said.

“Understanding how events like this shape people’s beliefs is key to guiding public health policy and future tobacco control strategies,” Mr. Wu said.

Although e-cigarettes are not harmless, Dr. Gerber added, clinicians widely consider them a less harmful alternative to conventional cigarettes. Research has shown that using e-cigarettes to help quit smoking increases the chances of success compared with other nicotine replacements such as patches, lozenges, and gum when combined with behavioral therapy. Negative public perceptions of e-cigarettes might steer people away from using them as a smoking cessation tool or encourage them to choose conventional cigarettes over e-cigarettes, a topic the team plans to explore in future research.

“Our findings show the need to strike a balance in public health messaging that discourages youths from using either product while also ensuring that adults who do smoke have access to accurate information about product risks and cessation options,” Dr. Thomas said.

Other UTSW researchers who contributed to this study are Sandi L. Pruitt, Ph.D., M.P.H., Professor in the O’Donnell School of Public Health and Associate Director of the Office of Community Outreach and Engagement in the Simmons Cancer Center; Chul Ahn, Ph.D., Professor in the O’Donnell School of Public Health and Director of the Biostatistics Shared Resource Core in the Simmons Cancer Center; David Balis M.D., Professor of Internal Medicine; John D. Minna, M.D., Director of the Hamon Center for Therapeutic Oncology Research, Professor of Internal Medicine and Pharmacology, and co-leader of the Experimental Therapeutics Research Program in the Simmons Cancer Center; and Sumin Son, B.A., and Matthew Lee, B.S., medical students.

Dr. Gerber holds the David Bruton, Jr. Professorship in Clinical Cancer Research.

This study was supported in part by the Harold C. Simmons Comprehensive Cancer Center Biostatistics Shared Resource (5P30 CA142543).