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The University of Cincinnati Cancer Center is committed to developing the next generation of cancer researchers and providers. The Trainee Associate Membership Program offers trainees access to tools and resources to help them be productive and successful cancer researchers and professionals. Trainee Associate Members have access to a community of cancer trainees and mentors, pilot grants, seminar series and educational events, career development opportunities, and more. There are numerous benefits offered to Trainee Associate Members, including:
In the most recent cycle, four Cancer Center Trainee Associate Members were selected for pilot project, travel and paper of the year awards. Congratulations to all the awardees!
Paula Saez-RaezTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Courtney Jones, PhD
The poor survival rates are largely due to relapse driven by treatment-resistant leukemia stem cells (LSCs). These cells depend heavily on oxidative phosphorylation (OxPhos) for energy production. However, directly targeting OxPhos has proven too toxic in patients, highlighting the need to identify safer mechanisms that regulate this process in LSCs.
“Our research focuses on glutathionylation, a reversible protein modification in which glutathione is temporarily added to oxidized cysteines during oxidative stress caused by cellular processes or AML therapies,” explained Paula Saez-Raez, a trainee associate member of the Cancer Center. “This modification protects proteins from damage and may help LSCs survive treatment. Because glutathionylation can impair protein function, it must be reversed through deglutathionylation once stress resolves. This process is partly regulated by the mitochondrial enzyme glutaredoxin 2 (GLRX2).”
Glutaredoxin 2 (GLRX2) is a crucial, glutathione-dependent enzyme that maintains cellular redox balance, repairs oxidative damage through reversible deglutathionylation and is essential for regulating energy metabolism, preventing cell death and protecting against tissue damage.
Saez-Raez and her team found that GLRX2 is overexpressed in LSCs compared to healthy hematopoietic stem and progenitor cells (HSPCs). Depleting GLRX2 impaired energy production and leukemia cell survival while largely sparing healthy cells, suggesting a selective vulnerability in AML. Proteomic analyses identified Argininosuccinate Synthase 1 (ASS1), a key enzyme in arginine metabolism, as a target of GLRX2. Stable isotope tracing further showed disrupted arginine metabolism and reduced creatine levels in GLRX2-depleted AML cells.
“Because creatine supports cellular energy balance and AML survival, we hypothesize that GLRX2 sustains LSC function by regulating mitochondrial protein glutathionylation and arginine metabolism to support OxPhos,” she said. “By defining how GLRX2 supports treatment-resistant leukemia cells, this work could provide the foundation for developing new therapies that specifically target LSCs while minimizing harm to healthy blood cells. Ultimately, this approach has the potential to reduce relapse and improve long-term outcomes for patients with AML.”
Kimia AbediTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Riccardo Barrile, PhD
Glioblastoma (GBM) is an aggressive brain cancer characterized by a complex tumor microenvironment that contributes to treatment resistance. While three-dimensional (3D) tumor models are critical for studying this biology, traditional manual culture methods often produce inconsistent results due to variability in handling and tumor architecture. These limitations reduce the reliability of high-throughput drug screening, where standardized models are essential.
“To address this challenge, we developed and validated an automated 3D bioprinting platform designed to generate consistent, patient-derived GBM tumor models,” shared Kimia Abedi, a trainee associate member of the Cancer Center. “We engineered a shear-thinning biomimetic bioink optimized for the precise placement of intact tumor spheroids. Compared with manual methods, bioprinting provided greater control over cell distribution, structural integrity, and reproducibility.”
The bioprinted constructs maintained high cell viability, supported tumor cell growth, and preserved hypoxic core regions, key features of GBM biology. Importantly, the models retained cancer stem cell characteristics and prevented the phenotypic changes commonly observed in conventional culture systems. While spheroids grown in standard Collagen I scaffolds lost expression of the stem cell marker CD44, bioprinted constructs maintained this clinically relevant feature.
“To evaluate compatibility with high-throughput screening, we performed temozolomide (TMZ) sensitivity testing,” she explained. “The bioprinted models generated reproducible dose-response data and accurately reflected the treatment resistance observed in the original patient tumors. The models also demonstrated adaptive metabolic responses to therapeutic stress.”
These findings establish an automated 3D bioprinting platform that overcomes key limitations of traditional 3D culture methods. By preserving tumor biology and enabling reliable drug screening, this technology provides a robust and translationally relevant tool for biomarker discovery and the development of personalized treatment strategies for resistant glioblastoma (GBM).
“By creating a standardized platform for drug screening, this technology can accelerate the identification of promising therapies, support biomarker discovery, and help researchers evaluate treatment strategies more efficiently,” Abedi said. “Ultimately, this approach advances the goal of personalized medicine by providing a more accurate and clinically relevant system for testing therapies and identifying the treatments most likely to benefit individual patients with glioblastoma.”
With this TAM Travel Award, Abedi was able to travel to Washington, DC to present this research at the 2026 Microphysiological Systems World Summit—an international conference highlighting bioengineering breakthroughs for recreating human organ architecture, function and disease modeling in vitro.
Sara Alharbi, MSTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Timothy Le Cras, PhD
The RAS gene encodes a family of small GTPase proteins that act as molecular switches, regulating critical cellular processes, including growth, survival and division. When mutated, RAS is one of the most common oncogenes in cancer, causing cells to grow uncontrollably. Additionally, mutations in RAS genes have been identified in several vascular anomalies, including kaposiform lymphangiomatosis (KLA).
Kaposiform lymphangiomatosis (KLA) is an extremely rare and aggressive disorder of the lymphatic system. It involves the abnormal growth of lymphatic vessels, which leak fluid around vital organs like the lungs and heart, causing bleeding issues, respiratory distress and blood clotting complications.
“Current treatment options are limited, and many patients do not respond adequately to available therapies,” said Sara Alharbi, a trainee associate member of the Cancer Center. “In this study, we evaluated RMC-7977, a new drug designed to directly inhibit RAS activity. Using laboratory models of KLA, we tested whether blocking RAS could reduce the abnormal behavior of cells carrying the NRASQ61R mutation, one of the most common mutations identified in affected patients.”
Alharbi and her team found that RMC-7977 effectively reduced the signaling pathways that drive disease progression. Treatment decreased abnormal cell growth and migration, restored more normal cell characteristics and lowered the production of molecules that promote abnormal blood vessel formation. The drug also prevented the development of enlarged vascular structures in an experimental model of angiogenesis.
“These findings suggest that RMC-7977 targets the underlying genetic cause of disease rather than simply treating symptoms,” Alharbi explained. “By directly inhibiting mutant RAS signaling, this approach may provide a more effective and precise treatment option for patients with KLA and other RAS-driven vascular anomalies. Ultimately, this work supports the continued development of targeted therapies for patients who currently have few effective treatment options.”
With this TAM Travel Award, Alharbi was able to travel to Philadelphia, PA to present this research at the 2026 International Society for the Study of Vascular Anomalies (ISSVA) World Congress—a hybrid multidisciplinary forum covering the latest advances in research, genetics, diagnostics and clinical care for vascular anomalies.
Levi FoxTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Susan Waltz, PhD
Breast cancer is the second leading cause of cancer-related death in women in the United States, with approximately one in eight women receiving a diagnosis in their lifetime. Understanding the mechanisms that drive aggressive breast cancer is critical for identifying new therapeutic targets and improving patient outcomes.
Receptor tyrosine kinases (RTKs) are high-affinity, cell-surface transmembrane receptors that act as catalysts to regulate fundamental cellular processes, including growth, division and metabolism. RTK signaling is a major driver of breast cancer progression, but its role in suppressing the tumor's innate immune response remains poorly understood.
“In this study, we investigated aggressive breast cancers that express the receptor tyrosine kinase RON and identified a key mechanism that allows these tumors to suppress innate immune signaling,” explained Levi Fox, a trainee associate member of the Cancer Center. “We found that RON increases the activity of TREX1, an enzyme that limits the production of type I interferons, molecules that help the body recognize and respond to cancer cells.”
TREX1 is a key DNA-degrading enzyme that acts as an “innate immune checkpoint.” Cancer cells often exploit it to evade the immune system by destroying stray cytosolic DNA, which would otherwise trigger the cGAS-STING pathway to spark an anti-tumor immune response.
“Our findings show that TREX1-mediated immune suppression promotes tumor growth and supports characteristics associated with breast cancer stem cells, which are linked to disease progression and treatment resistance,” said Fox. “Importantly, disrupting TREX1 activity restored anti-tumor immune signaling and reduced aggressive tumor behaviors in preclinical models.”
This research highlights TREX1 as a potential biomarker of aggressive breast cancer and identifies the RON-TREX1 pathway as a promising therapeutic target. By restoring the tumor's innate immune response, future treatments based on these findings may help slow tumor growth, reduce metastasis and improve outcomes for patients with aggressive forms of breast cancer.
As the project continues to uncover new insights into the role of innate immune signaling in breast cancer, Fox looks forward to sharing these findings with the broader scientific community while continuing to build the skills and collaborations needed to advance the research.
“Past and current support from the Cancer Center has been instrumental in advancing this research and providing opportunities to share my work with experts in the field,” said Fox. “In addition to funding, the Cancer Center’s training and professional development resources offered through the Trainee Associate Membership Program have helped me grow as a scientist. This travel award will allow me to present my research, receive valuable feedback and expand my professional network while fostering new collaborative opportunities.”
With this TAM Travel Award, Fox is able to travel to Louisville, KY to present this research at the 2026 FASEB Science Research Conference on Cell Signaling in Cancer—an event exploring basic mechanisms of signal transduction, therapeutic targeting of cancer cell signaling pathways and translational research from bench to clinic.
Kaposiform lymphangiomatosis (KLA) is an extremely rare and aggressive disorder of the lymphatic system. It involves the abnormal growth of lymphatic vessels, which leak fluid around vital organs like the lungs and heart, causing bleeding issues, respiratory distress and blood clotting complications. KLA is frequently associated with NRASQ61R mutations, and treatment options remain limited.
“Because this mutation hyperactivates the MAPK signaling pathway, we evaluated the effectiveness of three MEK inhibitors—trametinib, selumetinib and cobimetinib—in human endothelial cells (ECs) expressing NRASQ61R,” explained Sara Alharbi, a trainee associate member of the Cancer Center. “We also used RNA sequencing to identify genes altered by the mutation and determine which changes were reversed by trametinib.”
As first author on the study, Alharbi led the design and execution of the research. Through extensive laboratory and preclinical studies, she and her team found that trametinib was more effective than selumetinib and cobimetinib at reducing ERK activation, cell proliferation, migration, abnormal spindle-shaped morphology and ANG-2 production.
In addition to demonstrating trametinib's therapeutic potential, Alharbi played a key role in analyzing and interpreting the data to better understand the molecular mechanisms driving disease progression. Her work identified dysregulated Notch signaling as an important downstream effect of the NRASQ61R mutation and helped define how trametinib suppresses key disease-driving pathways and abnormal vascular growth. Through her leadership in study design, data analysis and manuscript preparation, Alharbi helped advance findings that support trametinib as a promising targeted therapy for patients with NRASQ61R-driven KLA.
For Alharbi, the opportunity to share these findings with the broader scientific community reflects both the impact of the research and the support she has received throughout her training.
“This award is an honor that recognizes the dedication, mentorship and collaboration that have shaped my scientific journey,” she said. “It motivates me to continue pursuing translational research that can improve outcomes for patients with rare vascular diseases, and I couldn’t have done it without the Cancer Center. The Trainee Associate Membership Program has provided invaluable mentorship, funding opportunities, scientific feedback and professional development resources that strengthened both my research and career growth.”
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