Huntsman Cancer Institute discovery innovations winter 2025

Breakthrough trial shows promising therapy for aggressive brain cancer
Huntsman Cancer Institute at the University of Utah (the U) participated in a clinical trial that found that a new combination treatment plan helped people with recurrent grade 3 astrocytoma, an aggressive form of brain cancer, live longer.

Howard Colman, MD, PhD, co-leader of the Neurologic Cancers Disease Center at Huntsman Cancer Institute and Jon M. Huntsman Presidential Professor of Neuro-Oncology at the U, is the principal investigator of the STELLAR study. The phase 3 trial, funded by Orbus Therapeutics, evaluated the efficacy and safety of a treatment plan using a combination of the drug eflornithine, a compound that targets an enzyme to inhibit the proliferation of tumor cells, and the oral chemotherapy lomustine, which is used to treat a variety of brain cancers. The study initially enrolled patients who were diagnosed with anaplastic astrocytoma. As tumor classifications changed, the study ended up including three types of brain tumors: glioblastoma, grade 3 IDH-mutant astrocytoma, and grade 4 IDH-mutant astrocytoma.  

The study results, published in the Journal of Clinical Oncology, found no difference in overall survival rates between the control and experimental groups among all patients. But for patients with the specific diagnosis of grade 3 IDH-mutant astrocytoma, the new treatment helped them live much longer—about 35 months compared to 24 months.
 
“Astrocytoma is an extremely challenging diagnosis for both patients and physicians, as the range of treatments and efficacy is limited,” says Colman. “It’s incredibly rewarding to be involved in a study like STELLAR, which demonstrated a combination treatment that has a significant benefit and offers incredible potential for patients with this specific diagnosis.”  

Study links high lipid counts to breast cancer, warns against keto diet
Huntsman Cancer Institute investigators Keren Hilgendorf, PhD, assistant professor of biochemistry at the U, Amandine Chaix, PhD, assistant professor of nutrition and integrative physiology at the U, and Greg Ducker, PhD, assistant professor of biochemistry at the U, have found that triple-negative breast cancer is fueled by lipids and that these fatty acids are a key feature of obesity that promotes tumor growth. Their National Cancer Institute-funded research, conducted in preclinical mouse models, suggests that breast cancer patients and survivors with obesity could benefit from lipid-lowering therapies—and that they should avoid high-fat weight loss regimens like ketogenic diets.   

“If we can target these high levels of fat in the blood, the cancer suffers because the lipids are no longer feeding the cancer,” says Hilgendorf. “But while our results in mice were striking, there are clear limitations in directly projecting these findings onto human patients. More research using human samples and patients will be necessary to confirm our hypotheses.”

Their findings, published in Cancer & Metabolism, could impact how breast cancer patients and survivors with obesity approach weight management. Clinicians often recommend patients lose weight as part of their treatment, as obesity can be a factor in increased risk of cancer spread or disease recurrence. The research team’s findings suggest the high-fat keto diet could have unintended side effects in this patient population—possibly causing tumors to grow.

New urban—rural—frontier classification system aims to better serve isolated communities
For many frontier patients, cancer care begins with an hours-long drive. This population faces unique challenges, like longer travel times, fewer available services, and greater delays in care. But they are often grouped together with other rural communities that are considerably closer to services.  

Researchers at Huntsman Cancer Institute have developed a new urban—rural—frontier classification system to better understand and address challenges faced by rural and frontier communities. Jennifer Doherty, PhD, MS, Huntsman Cancer Institute investigator, co-leader of the Cancer Control and Population Sciences Program, and professor in the Department of Population Health Sciences at the U, and Brody Gibson, doctoral candidate in the Department of Population Health Sciences at the U, are the creators of the Integrated Metropolitan-to-Frontier Area Codes (IMFAC) system in partnership with collaborators at the U.S. Department of Agriculture.  

Doherty and Gibson’s new tool, introduced in the Journal of Rural Health, combines existing systems to, for the first time, categorize areas both by how isolated and far they are from major population centers. IMFAC separates rural communities into four categories, revealing important differences in population density and travel times, likely reflecting access to essential resources and services like cancer prevention services and health care. IMFAC hopes to provide researchers and policymakers with a clearer classification framework that will help guide decisions around resource allocation and outreach strategies. 

“Rural and frontier communities are not all the same. By capturing the nuances of distance, IMFAC helps ensure that we can address the challenges these communities face,” says Doherty. “Understanding these differences is incredibly important to Huntsman Cancer Institute and the area we serve." 

Collaborative study finds melanoma-linked gene mutation in healthy skin
Robert Judson-Torres, PhD, Huntsman Cancer Institute investigator and associate professor of dermatology at the U, and a research team from the University of Queensland have found that a genetic mutation that causes melanoma also appears in healthy, unblemished skin, challenging prevailing ideas about the onset of the disease.  

Melanoma, the deadliest form of skin cancer, is often formed by a mutation of the BRAF gene in skin cells known as melanocytes. Judson-Torres says it was previously understood that the BRAF mutation only existed in moles and melanoma—not in normal skin.  

He and co-principal investigator Mitchell Stark, PhD, associate professor at the University of Queensland Frazer Institute, analyzed 97 skin samples taken from near a mole or where melanoma had been removed in both sun-protected and sun-exposed skin. The results of their research, published in the British Journal of Dermatology, showed that low levels of BRAF were present in many types of normal-appearing skin.

“The mole that’s visible on the skin is just the tip of the iceberg of a large field of cells that has the same mutation. The difference is the cells haven’t changed their behavior at all as a consequence of that mutation,” says Judson-Torres. “So that tells us that it’s not the mutation itself that causes melanoma. It’s the BRAF mutation coupled with something else that causes the cell to change how it’s behaving.” 

These federally supported efforts could also influence approaches to prevention, with the hope that clinicians can map these melanocyte fields and provide more targeted screening.  

Researchers identify drug that could halt growth of rare soft-tissue cancer
A collaboration between researchers at Huntsman Cancer Institute and Virginia Commonwealth University’s (VCU) Massey Comprehensive Cancer Center has identified a drug that could effectively treat synovial sarcoma, a rare and aggressive cancer that forms in the soft tissue of the body. The disease is commonly diagnosed in children and young adults, and it is incurable once it has metastasized. 

Motivated by this clinical need, Kevin Jones, MD, leader of the Sarcoma Disease Center at Huntsman Cancer Institute and professor of orthopaedics at the U, co-led the federally funded project exploring the use of a targeted therapy to shut down the molecular processes that spur on the growth of this tumor.  

Synovial sarcoma is driven by the gene SS18::SSX, which is created by two chromosomes swapping arms. The mutation caused by SS18::SSX throws off normal cell regulation and leads to tumor growth. They found that tumor growth is aided by a process called SUMOylation.  Using the drug subasumstat (TAK-981), Jones and his VCU colleagues investigated the blocking of the SUMOylation pathway. In preclinical mouse and human cell line models, they found that subasumstat effectively shut down SUMOylation—and that synovial sarcoma was highly sensitive to the inhibitor. Jones says he hopes they can bring the drug into a clinical trial for synovial sarcoma patients in the near future. 

VCU Massey investigators Anthony Faber, PhD, and Senthil Radhakrishnan, PhD, are co-principal investigators. Their research has been published in Nature Communications.  

The critical research happening every day at Huntsman Cancer Institute is supported by the National Institutes of Health/National Cancer Institute, including cancer center support grant P30 CA042014, as well as Huntsman Cancer Foundation. 

In Other News:
Cornelia Ulrich, MS, PhD, chief scientific officer and executive director of the Comprehensive Cancer Center at Huntsman Cancer Institute and Jon M. and Karen Huntsman Presidential Professor in Cancer Research in the Department of Population Health Sciences at the U, has been voted vice president/president-elect of the Association of American Cancer Institutes, the organization representing the nation’s top cancer centers.

More inherited genes for cancer have been discovered at Huntsman Cancer Institute than anywhere else in the world—thanks to one of our most valuable resources, the Utah Population Database. Hear more in the latest episode of our podcast, Delivering a Cancer-Free Frontier. 

About Huntsman Cancer Institute at the University of Utah
Huntsman Cancer Institute at the University of Utah is the National Cancer Institute-designated Comprehensive Cancer Center for Utah, Idaho, Montana, Nevada, and Wyoming. With a legacy of innovative cancer research, groundbreaking discoveries, and world-class patient care, we are transforming the way cancer is understood, prevented, diagnosed, treated, and survived. Huntsman Cancer Institute focuses on delivering the most advanced cancer healing and prevention through scientific breakthroughs and cutting-edge technology to create pioneering cancer treatments beyond the standard of care today. We have more than 325 open clinical trials and more than 300 research teams studying cancer. More genes for inherited cancers have been discovered at Huntsman Cancer Institute than at any other cancer center. Our scientists are world-renowned for understanding how cancer begins and using that knowledge to develop innovative approaches to treat each patient’s unique disease. Huntsman Cancer Institute was founded by Jon M. and Karen Huntsman.