A University of Texas at Dallas bioengineering researcher has secured more than $1 million in grants from the Cancer Prevention & Research Institute of Texas (CPRIT) to advance therapies for solitary fibrous tumor (SFT), a rare cancer driven by gene fusions.
Dr. Yi Li (MS’18), now an assistant professor of bioengineering, said the funding is “transformative” as he builds his lab and accelerates research into cancers powered by fusion genes. His efforts extend work initiated during his postdoctoral years in the lab of Dr. Leonidas Bleris at UT Dallas.
SFT develops when the NAB2 and STAT6 genes fuse, producing aberrant signaling that triggers cancer-cell growth. Although the underlying cause of the fusion remains unknown, the fusion itself offers a direct molecular handle. Current clinical management typically relies on surgery to remove tumors and/or radiation, because no drug is specifically tailored to SFT.
Li’s team previously collaborated with Dr. Heather Hayenga, an associate professor of bioengineering at UT Dallas, whose leadership helped establish local SFT research. Hayenga died on April 5, and the CPRIT-funded projects are intended to continue that scientific legacy while expanding toward new therapeutic strategies.
In recent years, the research community—supported by UT Dallas efforts—has used gene-editing tools to create experimental models that clarify how the NAB2–STAT6 fusion sustains disease. Those models have also supported an interdisciplinary pipeline for therapy development.
CPRIT support includes two major awards for Li. In May, he received a $249,000 high impact/high risk grant (RP260816) aimed at developing a potential immunotherapy for SFT. Last fall, he obtained an $899,216 individual investigator award (RP260461) to pursue a fusion-silencing approach using antisense oligonucleotides.
Antisense oligonucleotides are short strands of synthetic genetic material designed to block the activity of cancer-driving gene fusions. In laboratory-grown tumor cells and in animal models, the team has shown that these strategies can reduce fusion-gene activity and weaken oncogenic signaling.
A practical challenge is delivery: dense tumor tissue can limit how therapeutic molecules penetrate the tumor interior. Li is collaborating with Dr. Jeremiah Gassensmith in chemistry and biochemistry to design an effective delivery route through outer tissue barriers.
Overall, the work could generate a framework not only for SFT but also for other fusion-driven cancers that share similar vulnerabilities in gene-fusion signaling.
Subject of Research: Solitary fibrous tumor (SFT) driven by NAB2–STAT6 gene fusions
Article Title: (Not provided in the provided content)
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Web References: https://www.cprit.texas.gov/grants-funded/grants/rp260816 ; https://www.cprit.texas.gov/grants-funded/grants/rp260461
References: (No full reference list provided beyond the grant links)
Image Credits: The University of Texas at Dallas
Keywords: solitary fibrous tumor, SFT, NAB2–STAT6, gene fusion, antisense oligonucleotides, immunotherapy, cancer immunology, translational research, targeted therapy, drug delivery
Tags: bioengineering cancer therapiescancer research legacy continuationCPRIT cancer research grantsfusion gene signaling pathwaysgene fusion molecular targetinggene fusion-driven cancersgene-editing cancer modelspersonalized cancer treatment strategiesrare cancer treatment developmentrare tumor clinical managementsolitary fibrous tumor researchUT Dallas cancer research
