“Using a combination of advanced techniques — including RNA sequencing, DNA methylation profiling and single-cell CITE-seq — we identified unique gene expression and epigenetic patterns in each model,” shared Wang. “Importantly, we discovered a rare group of leukemia stem cells (LSCs) in all models that express CD25 and EpCAM.”

CD25 is a cell-surface protein that plays a crucial role in immune response, and EpCAM is a protein found specifically on the surface of epithelial cells that plays a role in cell-to-cell adhesion and cell signaling.

“These molecular flags may help doctors detect high-risk patients earlier and design targeted therapies,” said Wang. “CD25 and EpCAM serve as surface markers for identifying leukemia stem cells (LSCs), which display distinct tRNA profiles that represent a potential therapeutic target. By targeting these LSCs, which drive relapse and resistance, this research could prevent AML recurrence.”

Intramural RON Expression Supports Metastatic Prostate Cancer Development Through PRDM1 Expression

Angelle Jones  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Susan Waltz, PhD

While the relative five-year survival rate for those diagnosed with either localized prostate cancer is nearly 100%, the survival rate for those diagnosed with metastatic prostate cancer is approximately 30%. This means that when the cancer is confined to the prostate, treatment is highly effective, but when it has spread to other parts of the body, i.e. metastatic prostate cancer, the prognosis is considerably worse. Advances in treatment options have led to improved survival rates for both localized and metastatic prostate cancer, but the difference in survival between the two stages remains significant.

“In metastatic prostate cancer (mPCa), RON expression is significantly elevated,” said Angelle Jones, trainee associate member of the Cancer Center and PhD student at the University of Cincinnati College of Medicine. “Therefore, understanding the role of RON within mPCa is critical for developing targeted therapies that can effectively eliminate metastatic disease.”

The protein RON is often found to be overexpressed in various types of cancer, and its overexpression is linked to cancer progression and poor patient outcomes. RON, a receptor tyrosine kinase, plays a role in cell signaling pathways that promote cell growth, survival and migration, which are all crucial for cancer development and spread. Although RON has been studied in the context of primary prostate cancer, its specific role in mPCa remains largely unexplored.

“Despite its strong link to aggressive disease, no therapies currently exist that directly target RON,” Jones shared. “This highlights the need to identify druggable pathways downstream of RON to disrupt its tumor-promoting signals. Our novel preliminary data suggests that RON controls the expression of PRDM1, a transcription factor, in prostate cancer cells. Blocking RAS signaling in RON-expressing metastatic prostate cancer cells reduces their ability to migrate — similar to what we see when PRDM1 is removed in these cells.”

These findings suggest that the RON protein may use the RAS/ERK pathway to increase PRDM1 levels and promote metastasis. The RAS/ERK pathway, also known as the MAPK/ERK pathway, is a fundamental signaling cascade involved in regulating cell growth, division and survival. Aberrant activation of the RAS/ERK pathway, often due to mutations in RAS or RAF genes, can drive uncontrolled cell growth and contribute to cancer development. Therefore, targeting this pathway is a promising strategy for cancer treatment.

“This proposal seeks to define the RAS/ERK axis as a critical downstream effector of RON in mPCa, offering a mechanistic basis for targeting this pathway to block metastasis in RON-positive prostate cancers,” said Jones.

Bioprinting a Model of Breast Cancer-On-Chip for Assessment of Drug Efficacy In Vitro

Kimia Abedi, MS  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Riccardo Barrile, PhD

Breast cancer accounts for one in six cancer-related deaths in women, largely due to its ability to spread and the complex nature of its tumor microenvironment. A major challenge in treatment is poor drug and immune cell penetration, often caused by resistance mechanisms like remodeling of the extracellular matrix (ECM). Although animal models remain common in cancer research, there is a growing need for human-relevant in vitro systems to better model tumor behavior and treatment response.

“My research focuses on building an in vitro model of breast cancer a chip that mimics the human tumor microenvironment,” shared Kimia Abedi, MS, trainee associate member of the Cancer Center and PhD student concentrating on bioengineering and cancer modeling at the University of Cincinnati College of Engineering and Applied Science. “Using advanced 3D bioprinting, I create patient-specific cancer tissues integrated with blood-vessel-like structures to study how therapies interact with tumors.”

Traditional drug testing often fails to predict how therapies will work in actual patients. This model bridges that gap by recreating the human tumor environment, helping to better predict treatment responses and guide personalized care.

“This model features a perfusable, endothelial-lined channel that mimics the tumor’s vascular interface, enabling controlled delivery of drugs and immune cells,” Abedi explained. “The tumor region is made up of patient-derived organoids assembled using a modular approach that allows for consistent, spatially organized tumor structures near the vascular channel via precise bioprinting.”

Early data has shown Abedi and her team that tumor assembloids in this model form a dense collagen I-rich layer, closely resembling the fibrotic barrier, i.e. extracellular matrix (ECM), seen in patients and known to limit treatment access.

“In this study, we will test whether targeted enzymatic breakdown of this collagen barrier using engineered collagenases can improve the delivery and effectiveness of two therapies: Nab-paclitaxel, a nanoparticle-based chemotherapy, and NK cell-based immunotherapy,” Abedi said. “This work aims to uncover how the ECM contributes to treatment resistance and support the development of personalized therapies for breast cancer patients based on their specific tumor biology.”

The proposed study is a key component of a larger initiative to develop more predictive, patient-specific cancer models. By combining bioprinting and microfluidics, the research recreates the complex tumor microenvironment to better understand barriers to effective therapy. As noted by Abedi, this study would not be possibly without the generous support from the TAM Pilot Project Award — an opportunity she sees as instrumental to both her scientific growth and the advancement of her project.

“This award marks an important milestone in my development as a cancer researcher,” she said. “It allows me to advance a novel Breast Cancer-on-Chip model that replicates critical aspects of the tumor microenvironment, including stromal barriers and vascular interactions. The Cancer Center’s support not only affirms the translational value of this work but also provides essential resources to generate preliminary data for future NIH funding. More broadly, it strengthens my commitment to developing human-relevant cancer models that can improve therapeutic predictions and reduce reliance on animal studies.”

Reflecting on the impact of her training experience, Abedi took a moment to emphasize how the Cancer Center has shaped both her research and professional development.

“Being a Cancer Center trainee has significantly enriched my research journey,” she shared. “It has connected me with a vibrant community of interdisciplinary cancer researchers and provided opportunities to present my work at various retreats and symposia. These experiences have helped refine my scientific communication, receive feedback from established investigators and align my project with translational cancer priorities. Additionally, the resources and mentorship provided through the Cancer Center have supported the technical and conceptual development of this breast cancer model.”

Travel Awardees

Inhibition of PHGDH Suppresses Mtor Signaling and Metabolic Reprogramming in TSC2-Deficient Lymphangioleiomyomatosis Cells

Evans Kwabena Abor  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Jane Yu, PhD

Lymphangioleiomyomatosis (LAM) is a rare, progressive neoplastic disease, primarily affecting women of childbearing age. This disease is driven by TSC1 or TSC2 mutations, leading to chronic mTORC1 hyperactivation and abnormal proliferation of smooth, muscle-like cells, i.e. LAM cells, in the lungs and lymphatic system.

Rapalogs — a class of drugs that act as inhibitors of the mTORC1 complex — like sirolimus, can stabilize lung function and suppress tumor growth, but are not curative. The effects of rapalogs are cytostatic, meaning that once treatment stops, the disease often returns. Given that mTORC1 is sensitive to nutrient availability, there is growing interest in targeting metabolic vulnerabilities as a strategy to induce LAM cell death and reduce disease progression.

“My research focuses on lymphangioleiomyomatosis (LAM), which over time, destroys healthy lung tissue and impairs breathing,” said Evans Kwabena Abor, trainee associate member of the Cancer Center and graduate assistant at the University of Cincinnati College of Medicine. “I study how LAM cells rely on specific nutrients to grow — particularly how they use a pathway that helps produce the amino acid serine. This pathway begins with an enzyme called PHGDH.”

Phosphoglycerate dehydrogenase (PHGDH) is an enzyme that plays a crucial role in the biosynthesis of the amino acid serine as it is the first enzyme in the serine synthesis pathway. PHGDH is often overexpressed in cancer cells, contributing to increased serine production and promoting cancer cell growth and proliferation.

“We found that PHGDH is highly expressed in pulmonary LAM lesions, and this enzyme not only helps build serine but also supports the energy-producing parts of the cell, helps make building blocks of DNA via stabilization of de novo nucleotide synthesis enzymes PRPS1&2, CAD and TYMS independent of methotrexate or DHFR inhibition and stabilizes a major tumor cell growth pathway called mTORC1,” Abor explained. “Inhibiting PHGDH causes LAM cells to break down and induces autophagy, particularly when used in combination with the existing mTOR inhibitor rapamycin. This finding reveals a promising new approach that could support LAM treatment and potentially other diseases that rely on similar growth and energy pathways.”

Attending and presenting research at prestigious conferences is a crucial step in advancing scientific discovery and fostering collaboration. TAM Travel Awards are more than just financial support as they offer trainees this crucial opportunity, marking a meaningful step toward their future in cancer research.

“Receiving a TAM Travel Award is an important milestone in my academic and professional journey,” Abor said. “It allows me the opportunity to present my research at the AACR Annual Meeting, one of the most impactful gatherings in cancer research globally. This not only supports the dissemination of my findings to a wide scientific audience but also fosters exposure to cutting-edge advances in cancer biology. Additionally, this recognition motivates me to continue pursuing therapeutic discovery for difficult-to-treat tumors and brings me one step closer to my long-term goal of becoming a physician-scientist in oncology. It also provides a platform to elevate rare diseases like LAM, which often receive limited attention despite their profound clinical impact.”

Reflecting on the impact of his experience, Abor also highlighted how being part of the Cancer Center’s TAM Program has shaped both his research focus and long-term career goals.

“Being a Cancer Center trainee has been instrumental in my scientific and professional growth,” he said. “Through mentorship, access to expert research presentations, and networking opportunities, I have been able to refine my research questions and broaden the translational impact of my work. The community fostered by the Center has helped me stay connected to the larger mission of improving cancer patient outcomes through innovation and collaboration. This recognition motivates me to continue pursuing therapeutic discovery for difficult-to-treat tumors and brings me one step closer to my long-term goal of becoming a physician-scientist in oncology.”

Targeting Receptor Tyrosine Kinases and Integrated Stress Response in Glioblastoma

Kate Von Handorf  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: David Plas, PhD

Glioblastoma (GBM) is the most common and aggressive malignant brain tumor in adults, with a median survival of less than 15 months. It is characterized by its rapid growth and tendency to invade surrounding brain tissue. While treatments like surgery, radiation and chemotherapy can help manage the tumor and extend life, most patients survive less than two years after diagnosis.

“Despite the fact that 56% of GBM tumors exhibit elevated receptor tyrosine kinase (RTK) signaling, there are currently no first-line targeted therapies addressing these pathways,” said Kate Von Handorf, trainee associate member of the Cancer Center and graduate research assistant at the University of Cincinnati College of Medicine. “One RTK of interest, AXL, is overexpressed in GBM and linked to poor prognosis and treatment resistance, making it a compelling therapeutic target.”

AXL receptor tyrosine kinase (RTK) is a protein that plays a crucial role in various cellular processes, including cell survival, proliferation and migration. During their study, Von Handorf and her team used patient-donated glioblastoma stem-like cell lines and found that inhibiting AXL causes a rise in ATF4.

ATF4 is a protein that acts as a transcription factor and is involved in cellular processes like stress responses, metabolism and cell survival. In simpler terms, ATF4 can be imagined as a cellular “stress manager.” A part of the integrated stress response (ISR), ATF4 senses when the cell is under pressure and then activates certain genes to help the cell manage the situation. However, if the stress isn’t resolved, it can also lead to cell death.

“We found that AXL inhibitors activate a stress-sensing protein called GCN2, which triggers the integrated stress response by modifying another protein and increasing ATF4,” shared Von Handorf. “When we blocked GCN2, the stress response caused by AXL inhibitors went away, showing that GCN2 plays a central role.”

Similar to ATF4, GCN2 is a protein kinase that acts as a cellular stress sensor, and it plays a crucial role in the integrated stress response.

“Our early results show that blocking both AXL and GCN2 together enhances GBM cell death, suggesting that ISR activation may be a resistance mechanism to AXL-targeted therapy,” Von Handorf said. “Our study shows that AXL inhibition triggers the ISR via GCN2, and that dual targeting of AXL and GCN2 may represent a promising therapeutic approach for GBM and potentially other cancers with similar stress-adaptive features.”

As her research uncovers a potential strategy to overcome resistance in glioblastoma treatment, Von Handorf is also taking meaningful steps in her professional development. Thanks to this TAM Travel Award, she is preparing to attend her first major scientific conference.

“This award provides me the opportunity to attend, and hopefully present, at my first conference — the 30^th annual Society for Neuro-Oncology Meeting,” she said. “This will allow me to showcase my research alongside highly respected CNS tumor researchers and to learn from members of this field. Furthermore, I can gain highly important clinical, translational and discovery science insights that will help me develop my own project.”

Reflecting on the support she’s received through the TAM Program, Von Handorf emphasized how it has strengthened both her research and her ability to share her work with the broader research community.

“As a 2024 Spring TAM Pilot Project Award recipient, the TAM Program given me the opportunity to apply for funding for my research and is now helping me travel to present results at one of the largest conferences that focuses on CNS tumors,” she said. “Additionally, my membership provides the printing of one poster each year, which is extremely helpful. I would highly recommend becoming a trainee associate member to all my colleagues!”

Global Transcriptomic Analysis Identifies a Proton Therapy-Specific Response in Patient-Derived Oral Cancer Organoids

Anna Kirstein, MSc, PhD  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Susanne Wells, PhD

Head and neck cancers are aggressive, often recurring and spreading quickly, and patient outcomes have remained largely unchanged for decades despite advances in medicine and research. Oral squamous cell carcinomas (OSCCs), a subtype, arise from the squamous epithelium, or tissue, of the oral cavity. Roughly half of OSCC patients undergo radiation therapy as part of their treatment.

“Traditional radiation relies on X-rays, which not only target tumors but also damage surrounding healthy tissue,” said Anna Kirstein, MSc, PhD, trainee associate member of the Cancer Center and research fellow at the University of Cincinnati College of Medicine. “This can lead to serious, often lifelong side effects — such as difficulty swallowing or speaking, facial disfigurement and even secondary cancers caused by the radiation itself.”

To improve both treatment outcomes and quality of life, researchers are exploring new radiation approaches and sensitizers. One promising method is proton therapy, which can deliver radiation more precisely to tumors while sparing healthy tissues.

“In this study, we use patient-derived OSCC organoids — 3D cell cultures that model real tumors — to compare the biological effects of proton versus X-ray therapy,” Kirstein shared. “We are analyzing how each treatment impacts gene expression and cellular metabolism, with the goal of identifying biomarkers of response and discovering proton-specific sensitizers that could enhance therapy.”

By examining how tumor cells respond at both the genetic and metabolic levels, Kirstein and her team hope to uncover key biological markers that predict treatment effectiveness. These insights could guide the development of combination therapies that enhance the precision and power of proton radiation while also reducing harm to healthy tissue.

“Ultimately, this research aims to inform more effective and less toxic treatment strategies, tailored to individual patients,” she said. “Because our organoid models reflect real patient biology, these findings may also be relevant for other cancers where radiation remains a standard treatment.”

Attending and presenting research at prestigious conferences is a crucial step in advancing scientific discovery and fostering collaboration. Thanks to the TAM Travel Award, Kirstein will be able to take this step forward in her career by attending the 71^st annual Radiation Research Society Meeting.

“Receiving this award provides the opportunity to present and discuss my work to an international audience of experts,” she said. “In order to achieve my career goal of becoming an independent scientist, I need to build a strong foundation and network in the radiation community to expand my research and professional skillsets. I believe that attending the Radiation Research Society’s meeting will be pivotal in building strong connections and collaborations.”

Reflecting on the impact of the TAM Program, Kirstein highlighted how the experience has strengthened her research and expanded her professional network.

“The Cancer Center’s TAM Program has been an invaluable part of my cancer research journey,” she shared. “This program has connected me to a community that strives for excellence in cancer care, research, training and community impact. I’ve gained access to a supportive network of cancer researchers and professionals, as well as opportunities for collaboration, professional development and research funding. These resources have empowered me to grow professionally and share my research with audiences far beyond my home institution.”

Men1 Mediates Homeostasis in the Exocrine Pancreas in Response to Oncogenic Stress

Makenzie Fourman  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Amanda Wasylishen, PhD

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, originating from the cells lining the pancreatic ducts. With a five-year survival rate of only 13%, PDAC is a highly aggressive malignancy with a poor prognosis due to late detection and limited response to treatments.

Recent findings have revealed that what appears to be “normal” pancreatic tissue often harbors numerous precancerous lesions called pancreatic intraepithelial neoplasias (PanINs). Many of these lesions carry mutations commonly found in PDAC, yet the mechanisms that prevent their progression to cancer remain poorly understood.

“Our lab has found that Men1, a known tumor suppressor, is critical for keeping the pancreas healthy, especially during inflammation or when cancer-driving Kras mutations are present,” said Makenzie Fourman, trainee associate member of the Cancer Center and graduate assistant at the University of Cincinnati College of Medicine. “In mice with both a Kras mutation and loss of Men1, the pancreas shows widespread signs of early cancer development, suggesting that Men1 helps prevent tumor formation. We believe Men1 protects the pancreas by helping cells stay stable under stress.”

To test this hypothesis, Fourman and her team used single-nucleus RNA sequencing to study pancreas tissue from genetically engineered mice both with and without Men1, before visible tumors appeared. They identified 19 different cell types and found major gene changes in acinar cells, especially in genes linked to cell movement and invasion.

“To study Men1’s role further, we created cell lines from Men1-deficient mice and reintroduced Men1 using a virus,” Fourman explained. “We're now applying this research to human pancreatic cancer cells, including a line that carries a Men1 mutation and doesn’t make Menin protein. Our results show that loss of Men1 leads to increased expression of over 600 genes tied to invasive behavior — findings that match patterns seen in human pancreatic cancers with low Men1 expression. We’re now working to understand how these gene changes occur and what they mean for cancer development in people.”

In summary, Men1 is essential for maintaining healthy pancreatic cells and preventing early stages of cancer, especially when KRAS mutations are present. Learning more about how Men1 works could lead to new ways to stop pancreatic cancer before it starts.

As Fourman’s research continues to uncover critical insights into how pancreatic cancer develops at its earliest stages, this award marks an important step in amplifying that impact. It offers not only recognition, but also the opportunity to connect with the broader scientific community and advance her long-term goals.

“This award provides an invaluable opportunity to present these findings to a diverse and knowledgeable audience, inviting fresh perspectives and stimulating the kind of scientific exchange that drives innovation and progress,” she shared. “Additionally, this award enhances my ability to build connections with principal investigators in the cancer research field as I explore potential postdoctoral opportunities. Securing a postdoctoral position is an essential step toward my long-term goal of becoming a faculty member at a smaller academic institution, where I hope to lead a research lab and mentor the next generation of scientists.”

Novel Replication Factors in Maintaining AML Cell Fate

Xiaoqin Zhu, MS, MD  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Andrew Volk, PhD

Acute myeloid leukemia (AML), the most common type of acute leukemia in adults, is an aggressive and difficult-to-treat blood cancer in which the bone marrow makes a large number of abnormal blood cells. Despite the use of intensive chemotherapy and bone marrow transplantation, treatment outcomes remain poor, with a five-year survival rate of approximately 30%. A major reason for treatment failure is our limited understanding of how AML develops, along with a lack of therapies that can effectively treat all patients. To address this gap, there is an urgent need to investigate the molecular mechanisms that drive AML.

AML often starts with mutations in genes that control how DNA is packaged and read, which blocks normal myeloid cell development and causes immature cells (myeloblasts) to grow uncontrollably. Forcing these cells to fully mature is a promising way to treat the disease, but current therapies can’t reliably do this. One potential approach is to target replication-related proteins, since key decisions about cell identity happen during DNA replication.

“Using a technique called iPOND mass spectrometry, I discovered that HNRNPL — a protein known for its role in mRNA splicing and cancer — is also involved in DNA replication and helps maintain the identity of leukemia cells,” explained Xiaoqin Zhu, MS, MD, trainee associate member of the Cancer Center and graduate assistant at the University of Cincinnati College of Medicine. “Data from large cancer databases show that HNRNPL is highly active and essential in AML. When HNRNPL is removed from AML cells, they begin to mature and lose their ability to drive leukemia, both in lab experiments and in animal models. Importantly, this effect does not harm healthy blood stem cells, suggesting HNRNPL could be a promising treatment target.”

Building on these important discoveries, Zhu is eager to share her work with the broader cancer research community. The opportunity to present her findings at a national conference not only allows her to highlight HNRNPL as a novel therapeutic target in AML but also helps foster the professional growth necessary to advance her career.

“Receiving this travel award marks a pivotal moment in my academic and professional development, especially as an international trainee pursuing a career in cancer research,” she shared. “This recognition not only affirms the value of my scientific contributions but also provides a critical opportunity to present my work on a national platform, strengthening my communication skills and expanding the reach of my research.”

“Attending the 2025 Federation of American Societies of Experimental Biology & Hematologic Malignancies Conference allows me to engage directly with leading scientific, technological and clinical innovators, whose insights and feedback will help refine my work and inspire future directions,” Zhu continued. “Most importantly, this experience helps lay the foundation for meaningful collaborations and mentorships that will shape my transition into postdoctoral training and support my long-term goal of establishing an independent research program.”

Paper of the Year Awards

RAS Pathway Mutations and Therapeutics in Vascular Anomalies

Sara Alharbi, MS  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Timothy Le Cras, PhD

Vascular anomalies (VAs) are a diverse group of disorders characterized by the dysregulated growth of blood vessels, often leading to debilitating clinical outcomes, including hemorrhage, disfigurement, and organ dysfunction.

“Recent research has shown that mutations in RAS genes (KRAS, NRAS, and HRAS) play a key role in the development of many vascular anomalies by disrupting normal RAS/MAPK signaling,” said Sara Alharbi, MS, trainee associate member of the Cancer Center and graduate researcher at the University of Cincinnati College of Medicine. “Our study brings together current knowledge about how these mutations drive disease and examines new treatment options that target this pathway.”

In particular, Alharbi and her team are focusing on MEK inhibitors, which were originally created to treat cancer. MEK inhibitors are a class of targeted cancer therapies that block MEK1 and MEK2 proteins, which disrupts the MAPK/ERK pathway. Inhibiting this pathway can impair cancer cell proliferation and survival, potentially inducing apoptosis, or cancer cell death.

“As the first author of this study, I played a central role in conceptualizing, designing and executing the research,” shared Alharbi. “I conducted a comprehensive literature review to identify and analyze RAS pathway mutations (KRAS, NRAS, HRAS) implicated in vascular anomalies and evaluated preclinical models to illustrate how these mutations drive disease progression. I synthesized findings on MEK inhibitors as potential therapies and emphasized the translational potential of repurposing cancer drugs for rare vascular conditions.”

Beyond research and analysis, Alharbi played a critical role in shaping the final manuscript, ensuring the integrity and clarity of the scientific message.

“Additionally, I ensured the scientific rigor and accuracy of the final publication,” she said. “This work bridges molecular discovery and clinical innovation, laying the groundwork for precision therapies in patients with vascular anomalies.”

Targeting Hsp70 Immunosuppressive Signaling Axis with Lipid Nanovesicles: A Novel Approach to Treat Pancreatic Cancer

Ahmet Kaynak, MSc, PhD  Trainee Associate Member, University of Cincinnati Cancer Center Mentor: Xiaoyang Qi, PhD

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, accounting for over 80% of cases. While it is currently the fourth leading cause of cancer-related death in the United States, PDAC is predicted to become the second by 2023. Despite advances in treatment, PDAC remains one of the most lethal cancers, with a five-year survival rate of just 13%, largely due to its aggressive progression, early metastasis and delayed symptom onset that complicates early detection.

“Current treatments, like FOLFIRINOX or gemcitabine-abraxane, only extend survival by a few months in responsive patients, highlighting the urgent need for new therapies,” said Ahmet Kaynak, MSc, PhD, trainee associate member of the Cancer Center and postdoctoral fellow at the University of Cincinnati College of Medicine. “Our research focuses on a protein called Hsp70, which is secreted by cancer cells and helps suppress immune activity around the tumor. We found that a specially designed nanoparticle — SapC-DOPG — can block Hsp70’s actions and reduce tumor growth in mice. By targeting the tumor’s ability to shut down the immune system, we are developing a promising new form of cancer therapy.”

Hsp70, or heat shock protein 70, is a family of proteins that play crucial roles in various cellular processes, primarily by assisting in protein folding, preventing protein aggregation and aiding in protein degradation. Hsp70 is often overexpressed in cancer cells and is associated with tumor survival, drug resistance and metastasis.

“This study uncovers a previously unrecognized mechanism of immune escape in pancreatic cancer and proposes a promising immunotherapeutic approach,” Kaynak shared. “If translated into clinical practice, this strategy could enhance survival outcomes for patients with pancreatic cancer and may hold therapeutic potential for other malignancies exhibiting similar immune resistance pathways.”

Kaynak played a leading role in driving the project forward from concept to completion. His contributions spanned every stage of the research process, reflecting both scientific rigor and a deep commitment to advancing immunotherapeutic strategies.

“As the first author, I was responsible for the overall design and execution of the study,” he said. “This included formulating the research hypothesis, developing the methodology, conducting the experiments, analyzing the data and drafting the original manuscript. I also created the visualizations and coordinated the contributions from co-authors.”

More than a mark of achievement, this award represents a meaningful milestone in Kaynak’s career, affirming the importance of his research and pushing him forward on his path advancing immune-based treatments for pancreatic cancer.

“Being recognized for this work is an important milestone in my career,” he shared. “It reinforces the significance of our efforts to address one of the deadliest cancers — pancreatic ductal adenocarcinoma (PDAC) — and motivates me to continue pursuing innovative strategies in cancer immunotherapy. This award highlights our translational research potential and supports my goal of becoming an independent investigator dedicated to developing immune-based treatments for cancer.”