June 10, 2025 | Austin, Minn. — Diffuse midline glioma (DMG) is a particularly cruel form of cancer that begins in the brain or spinal cord, spreads aggressively, and affects mostly children—with no cure and no current effective options for treatment. After diagnosis, the median survival time for patients lingers around just one year. At The Hormel Institute, University of Minnesota, scientists are working to change this—and they have uncovered a newly discovered mechanism that drives the development of these nefarious tumors.
Researchers at The Hormel Institute used the gene-editing technology known as CRISPR to correct a cancer-causing genetic mutation, then used a technique known as live-cell imaging to compare cells with and without the mutation. They shared the results of their study in a paper recently published in Current Biology.
“The main takeaway is that there is a new, previously undiscovered mechanism that drives these tumors. Uncovering this will open up new avenues for diagnosis and treatment,” Professor Edward Hinchcliffe, PhD, who led the study, said. “We want to understand what goes wrong in these tumor cells to design treatment strategies so that patients and their loved ones have more options when navigating a difficult journey. This is what drives the work that we do.”
This work was a joint project with Associate Professor James Robinson, PhD. Additional researchers who contributed to the paper include Senior Scientist Charles Day, PhD; Post-Doctoral Fellows Florina Grigore, MD, Faruck L. Hakkim, PhD, and Souren Paul, PhD; Researcher 3 Alyssa Langfald; and Summer Undergraduate Research Experience (SURE) interns Molly Weberg, Sela Fadness, and Paiton Schwab.
The work challenges a long-held notion in the field of DMG biology that the cause of these tumors is exclusively epigenetic, or tied to behaviors and the environment that alter how DNA expresses itself.
A major driving factor in causing diffuse intrinsic pontine glioma (DIPG)—a form of DMG that is location-specific to the part of the brain stem known as the pons—influences the process of paired chromosomes separating during cell division. The researchers’ study revealed that a protein crucial to this process, called histone H3.3, undergoes a mutation that makes it “sticky” and unable to efficiently complete a necessary enzymatic reaction. What results are tumor cells that have “wildly different” numbers of chromosomes, which is thought to be a major cause of high-grade cancers, Dr. Hinchcliffe explained.
This research was funded by grants from the Department of Defense CDMRP Cancer Research Program, the National Institutes of Health, and the Minnesota Mayo Partnership Program. The work was awarded the Merit Mary Swenson Prize for DIPG Research at the Society for Neuro Oncology Annual Meeting.
Read the paper: https://doi.org/10.1016/j.cub.2024.11.035
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Founded in 1942 by The Hormel Foundation, The Hormel Institute, University of Minnesota, makes scientific advancements that enhance wellbeing and extend human life. For more than 80 years, we have pursued our mission to conduct research and provide education in the biological sciences with applications in medicine and agriculture. A part of the University of Minnesota's Research and Innovation Office, The Hormel Institute partners with the region's leading biomedical research facilities, including Mayo Clinic.