The University of Cincinnati Cancer Center Pilot Project Award Program is dedicated to advancing cancer research by providing pilot funding to our faculty investigators. The program is supported by generous contributions from the following partners: Marlene Harris Ride Cincinnati Cancer Research Fund, the Bergman Family Fund, the Steven Goldman Memorial Cancer Research Fund and the Appendix Cancer Research Fund.

The goals of the Pilot Project Award Programs are to:

• Increase collaborative interactions to foster innovative research.
• Facilitate novel approaches.
• Encourage the entry of new investigators into cancer research.
• Facilitate the translation of laboratory findings into clinical interventions.
• Generate preliminary data that will lead to peer-reviewed, cancer-relevant extramural funding, conference presentations and publications.

Ten Cancer Center members received funding for their pilot projects in the Spring 2025 cycle. Congratulations to all the awardees!

Leveraging Oncogenic Hijacking of PRPS Enzymes for Diagnostic and Therapeutic Potential

Tom Cunningham, PhD Associate Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center Associate Professor, Department of Cancer Biology University of Cincinnati College of Medicine

“Our project focuses on one of nature’s most highly controlled and evolutionary conserved metabolic enzymes — the phosphoribosyl pyrophosphate synthetase (PRPS)—which serves as the only thoroughfare that connects sugars to downstream nucleotide synthesis pathways,” explained Tom Cunningham, PhD, associate member of the Cancer Center and associate professor at the University of Cincinnati College of Medicine.

Phosphoribosyl pyrophosphate synthetase (PRPS), also referred to as ribose-phosphate diphosphokinase, is an enzyme that helps turn ribose 5-phosphate into phosphoribosyl pyrophosphate (PRPP), which is a key building block needed to make DNA and RNA. Cancer cells, however, possess numerous mechanisms to hyperactivate this enzyme, boosting nucleotide production to support their rapid and uncontrolled growth.

One version of this enzyme, PRPS2, is increased by the cancer-driving MYC gene — a proto-oncogene that plays a critical role in cell growth, division and apoptosis, or cell death. This gene encodes a transcription factor that regulates a wide array of genes involved in these processes. Deregulation of the MYC gene, often due to mutations or chromosomal translocations, can lead to uncontrolled cell growth and is connected to numerous cancers.

“Our previous work uncovered how oncogenes remodel the PRPS enzyme to drive cancer, and we developed ways to evaluate its composition,” Cunningham shared. “This award allows us to build on those findings by creating and refining a diagnostic test to measure PRPS activity in tumor samples. Our goal is to use this tool to guide personalized treatment, as changes in the enzyme’s activity can influence how cancer cells respond to different therapies, including their sensitivity to oxidative treatments and a new drug strategy that targets this unique enzyme function.”

The secondary aim of this project is to investigate how cancer-specific mutation in PRPS create exploitable metabolic weaknesses, particularly in relapsed/refractory acute lymphoblastic leukemia (ALL), i.e. leukemia that either returns after a period of remission (relapsed) or does not respond to initial treatment (refractory). Cunningham and his team will begin designing a metabolic engineering approach to leverage the elevated glucose uptake in tumors, enabling them to generate cytotoxic agents internally and destroy themselves from within.

“Metabolic reprogramming is a defining feature of cancer and represents a promising therapeutic window to selectively eliminate malignant cells while sparing healthy tissue,” said Cunningham. “The challenge, however, is figuring out how to turn theory into practice to achieve durable therapeutic efficacy. Our expertise tells us that there is no silver bullet that, on its own, disrupts the highly interconnected metabolic network of pathways that cancer cells employ. Our strategy seeks to strip away the flexibilities and redundancies within these networks to generate new cancer-specific vulnerabilities, thus providing a viable path to effectively target this core cancer hallmark.”

Reflecting on the value of collaboration and support, Cunningham noted how the Cancer Center’s support has helped accelerate his lab’s work.

“The Cancer Center’s Pilot Project Award Program facilitates the continuation of impactful studies our lab has been conducting, and it provides the resources to launch us into new directions that help us translate our basic science into clinically impactful diagnostic and therapeutic products,” he said. “Furthermore, Cancer Center membership presents researchers with a community focused on a shared goal of eradicating cancer. The exposure members have to different perspectives, strategies and communities of researchers is truly invaluable.”

HPV and You-A Collaborative Initiative through Innovation, Narratives, and Targeted Health Education (HYACINTH) to Enhance Knowledge and Attitudes on HPV Vaccination and Self-Sampling

Minjin Kim, PhD, MSN Member, Cancer Prevention, Control & Population Sciences Research Program University of Cincinnati Cancer Center Assistant Professor University of Cincinnati College of Nursing

Genital human papillomavirus (HPV) is a leading cause of cervical and other cancers. However, Korean American women have low rates of HPV vaccination and cervical cancer screening, even though both have proven to be effective prevention strategies. The recent FDA approval of HPV self-sampling offers a new way to increase screening, especially for those who face cultural or practical challenges with clinic visits.

Building on this opportunity, the HPV and You-A Collaborative Initiative through Innovation, Narratives, and Targeted Health Education (HYACINTH) pilot study aims to create and test a bilingual, web-based program tailored for Korean American women. The goal is to boost understanding, shift attitudes and encourage HPV vaccination as well as self-sampling.

“Building on my K23-funded study, which focuses on HPV vaccination by including HPV self-testing, this study aims to (1) explore the attitudes, barriers and benefits of HPV vaccination and testing through focus groups with 30–40 Korean American women, (2) utilize those insights to design the HYACINTH intervention, including clear information about HPV self-testing, and (3) determine the program’s feasibility and acceptability with feedback from participants and the Community Advisory Board to make improvements,” explained Minjin Kim, PhD, member of the Cancer Center and assistant professor at the University of Cincinnati College of Nursing.

By combining findings from the HYACINTH study with her expertise in digital health communication, Kim is taking a novel approach to cancer prevention. Leveraging storytelling and artificial intelligence (AI), this study will transform health education into a personalized experience, ensuring that culturally tailored content leads to meaningful behavioral changes.

“My research combines storytelling and artificial intelligence (AI) to create digital tools — such as chatbots — that deliver personalized, culturally relevant cancer prevention education,” said Kim. “These tools are designed to speak the user’s language, reflect their lived experiences and support preventive health actions, e.g. getting vaccinated or screened. While the current focus is on HPV-related cancers among Korean American women, this approach is designed to serve as a model that can be adapted to other diseases and applied to other underserved populations.”

By centering user experience and cultural nuance, this digital tool will not only inform but it will truly engage its users. Her long-term goal is to ensure these AI-driven resources can be tested, refined and ultimately implemented across diverse populations to improve cancer prevention outcomes on a wider scale.

“Everyone deserves access to cancer prevention tools that are culturally relevant and easy to use, which is why I focus on underrepresented communities, integrating primary and secondary prevention strategies,” she said. “The HYACINTH intervention is intentionally designed to be replicable and expandable to support broader disease prevention and reach other at-risk communities. This award really allows me to refine and test the feasibility and acceptability of this intervention, generate pilot data for a future R01 and further develop AI tools that are culturally grounded, scalable and designed for real-world implementation in underserved communities.”

For researchers like Kim, this award is more than just recognition — it’s a meaningful step forward in her mission to close the cancer prevention gaps present in the community.

“This award is both an honor and a critical investment in the future of my research as it validates the importance of using culturally responsive and AI-driven strategies to address cancer prevention disparities,” she said. “It also provides me the opportunity to expand my work beyond primary prevention through HPV vaccination to include secondary prevention with HPV self-sampling tests. This extension is essential for reaching underserved communities who may face barriers to traditional screening.”

“Additionally, my membership with the Cancer Center has been instrumental in expanding the scope and visibility of my work,” she continued. “The Cancer Center has provided pilot funding and interdisciplinary collaboration opportunities that have supported the development of the HYACINTH project and its alignment with cancer equity and implementation science priorities.”

Interrogating Therapeutic Response in AML Patients Harboring Non-Canonical BRAF Mutations

Linde Miles, PhD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center Researcher, Division of Experimental Hematology & Cancer Biology Cincinnati Children’s Hospital Medical Center

Acute myeloid leukemia (AML), the most common type of adult acute leukemia, originates from somatic mutations, which are acquired alterations in the DNA of cells that are not inherited from parents. These mutations happen specifically in hematopoietic stem and/or progenitor cells — the source of all blood cells, including red blood cells, white blood cells and platelets.

“We recently identified recurrent mutations in the BRAF gene, which encodes an integral kinase in the RAS/MAPK signaling pathway, in AML patients,” said Linde Miles, PhD, Cancer Center member and researcher at Cincinnati Children’s Hospital Medical Center. “Divergent from other cancers, the majority of BRAF mutations we identified were outside of the well-characterized V600 hotspot and therefore, non-canonical mutations.”

The BRAF gene is a human gene that encodes a protein involved in transmitting signals that regulate cell growth and proliferation. As a part of the RAS/MAPK pathway — a critical signaling pathway for cell function — mutations in the BRAF gene can lead to various health conditions, including cancer.

“While these mutations are frequently seen in certain subtypes of cancer, they are not typically seen in the blood cancer we study, acute myeloid leukemia (AML),” shared Miles. “Our clinical collaborators have shown that AML patients who harbor these mutations respond poorly to treatment, regardless of the treatment regimen, and tend to have significantly worse outcomes compared to patients with other RAS/MAPK mutations.”

This project aims to uncover how these mutations influence treatment response and promote resistance and to explore alternative treatments that may be more effective against BRAF-mutant AML. While BRAF mutations have been extensively characterized in other cancer types, their role in AML remains unclear. Given BRAF’s central function within the RAS/MAPK signaling pathway — a pathway frequently activated in cancer — uncovering how these mutations drive AML progression and therapy resistance could provide new insights not only into AML biology but also into cancers where BRAF alterations are more prevalent. Additionally, this investigation into novel therapeutic approaches may yield strategies applicable to other malignancies with similar molecular profiles.

“For this study to be competitive as a larger grant, though, we need more preliminary data, and this award allows us to do just that,” Miles said. “The Cancer Center has provided necessary opportunities for basic scientists, like me, and clinicians to discuss our work and find ways to collaborate, which helps drive discovery and impactful science.”

In addition to critical funding, Miles also highlighted how the collaborative environment fostered by the Cancer Center plays a key role in advancing research. By bringing together scientists from diverse disciplines, the Cancer Center encourages the exchange of ideas and supports innovative partnerships that might not otherwise occur. This spirit of collaboration strengthens both research outcomes and educational opportunities.

“My Cancer Center membership has enabled rich conversations and collaborations with researchers from a wide range of cancer specialties,” she said. “This has not only strengthened our research but also provided an outstanding training environment for our students. The funding opportunities exclusive to members—like the Spring Pilot Grant—have been instrumental in propelling our work forward.”

Feasibility of Oral Akkermansia Muciniphila Supplementation for Gastrointestinal Toxicity Mitigation During Pelvic Radiation

Bailey Nelson, MD Associate Member, Experimental Therapeutics Research Program University of Cincinnati Cancer Center Assistant Professor, Department of Radiation Oncology University of Cincinnati College of Medicine

Pelvic radiation therapy is a cancer treatment that uses high-energy rays to destroy cancer cells in the pelvic area — the lower part of the abdomen between the hips. This treatment is commonly used to treat gastrointestinal (GI), genitourinary (GU) and gynecologic malignancies. However, this treatment can lead to acute and chronic effects, like diarrhea, fecal urgency, abdominal cramping and malabsorption.

“The exact mechanism of gastrointestinal symptoms is elusive, but there is sufficient data to suggest that the intestinal microbiome plays a role in radiation-induced GI injury,” said Bailey Nelson, MD, associate member of the Cancer Center and assistant professor at the University of Cincinnati College of Medicine. “The microbiome likely plays a much larger role in cancer development and treatment toxicity than we ever imagined.”

A biome is a distinct ecosystem characterized by its environment and its inhabitants. The intestinal microbiome is a miniature biome populated by trillions of microorganisms, such as bacteria, viruses, fungi and parasites.

“The intestinal microbiome has both ‘good’ and ‘bad’ bacteria,” Nelson shared. “If we can find ways to manipulate and harness the microbiome to lessen treatment-related toxicity and decrease rates of cancer development and progression, it could be truly revolutionary. This is only the beginning.”

One such “good” bacterium is Akkermansia muciniphila — a beneficial bacterium that breaks down mucus in the intestines and helps maintain the intestinal lining.

“In preclinical data models, Akkermansia muciniphila, was protective of radiation-induced GI toxicity through enhancing intestinal epithelial repair,” explained Nelson. “In our previous institutional retrospective study, A. muciphila was enriched in patients with no-to-mild diarrhea after whole pelvic radiotherapy compared to patients with moderate-to-severe diarrhea, indicating that it may be protective against radiation-induced GI toxicity.”

In this Phase I feasibility trial, patients with gastrointestinal (GI), genitourinary (GU) and gynecologic cancers undergoing whole pelvis radiotherapy will be eligible to receive a 10-week course of A. muciniphila supplementation. The primary objective is to evaluate adherence and tolerability of the probiotic. As an exploratory aim, Nelson and her team will assess gastrointestinal toxicity outcomes, particularly diarrhea. Pending tolerability results, a randomized controlled trial will be designed to more rigorously evaluate its potential protective effects.

To move this promising concept forward, Nelson applied for support through the Cancer Center’s Pilot Project Award Program. Designed to empower early-stage investigators, the program provides both funding and mentorship to help researchers develop their ideas into full-scale clinical studies. For Nelson, the award offered a unique opportunity to gain hands-on experience with designing and launching a clinical trial, while also building essential skills in grant writing and research collaboration.

“As an early-stage investigator (ESI), it can sometimes be difficult to find resources and funding due to inexperience and lack of support,” she said. “The Cancer Center’s Pilot Project Award Program encourages new investigators to apply with the support of a senior mentor. Through this process, under the guidance of my mentor, I am learning how to write grants, design Phase I clinical trials, create research budgets, collaborate with various colleagues and consultants, and more. I am extremely grateful for this educational opportunity from and the support of the Cancer Center.”

Promoting Anti-Tumor Macrophage Differentiation for Glioblastoma Immuno-Oncology

David Plas, PhD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center Professor, Department of Cancer Biology University of Cincinnati College of Medicine

Glioblastoma (GBM), the most common primary brain cancer in adults, is a highly aggressive brain tumor that is characterized by rapid growth and frequent invasion of surrounding brain tissue. Established in 2005, standard treatment includes surgery, radiation and the chemotherapy drug temozolomide (TMZ). In nearly 20 years, there has been little progress, and despite major advances in other cancers, no targeted or immunotherapy drugs have been approved for GBM.

“Our strategy holds promise for a twofold therapeutic effect in glioblastoma — disrupting cancer growth and priming the immune system to better recognize and destroy tumor cells,” shared David Plas, PhD, Cancer Center member and professor at the University of Cincinnati College of Medicine. “Despite advancements in immunotherapy, glioblastoma (GBM) remains resistant to immune activation. Emerging data highlight macrophages as the dominant immune cell type in GBM. Our goal is to ‘reprogram’ these macrophages from a tumor-promoting to a tumor-fighting state by blocking the AXL protein.”

Macrophages are a type of white blood cell that surrounds and kills microorganisms, removes dead cells and stimulates the action of other immune system cells. The AXL receptor tyrosine kinase (AXL) is a member of the TAM family of receptor tyrosine kinases (RTKs) that plays a role in various cellular processes, including cell survival, proliferation, migration and differentiation. It is also known as a potential therapeutic target in cancer due to its involvement in tumor progression, metastasis, and drug resistance. The AXL protein is often overexpressed in GBM and contributes to tumor invasiveness, chemoresistance and poor survival.

“This proposal advances our ongoing research into AXL inhibition as a therapeutic approach for glioblastoma (GBM),” said Plas. “In our earlier studies, we identified AXL as a contributor to glioblastoma (GBM) growth and therapy resistance, and AXL inhibitors have shown effectiveness in preclinical models and can reach brain tissue. Since AXL also promotes an immune-suppressive tumor microenvironment, this study will explore how blocking AXL affects immune responses in GBM using patient-donated tumor samples, with the goal of informing future immunotherapy strategies.”

To carry this research forward, Plas and his team are leveraging a range of resources and expertise made available through the Cancer Center. These tools not only allow for a deeper understanding of AXL’s role in driving glioblastoma progression and immune evasion but also support the integration of high-resolution imaging and advanced genomic analysis into the study. This multidisciplinary approach strengthens the team’s ability to examine how AXL-targeted therapies may reshape the tumor microenvironment and improve immune responses.

“Thanks to the Cancer Center, we can take a major step forward in our investigation into the immunosuppressive role of macrophages in glioblastoma progression,” he said. “Furthermore, the Cancer Center makes advanced research capabilities accessible for our laboratory. Access to the UCCC Biospecimen Repository enables us to study patient-derived brain tumors, ensuring our findings reflect real-world disease biology. Advanced microscopy support allows high-throughput imaging of tumor responses to novel treatments, while our collaborative efforts in single-cell transcriptomics will help define the role of AXL inhibition in reprogramming glioblastoma-associated macrophages.”

Increasing the Utilization of Lung Cancer CT Screening to Promote Health for All Patients

Robert Van Haren, MD, MSPH Member, Experimental Therapeutics Research Program University of Cincinnati Cancer Center Associate Professor, Department of Surgery University of Cincinnati College of Medicine

In 2025, it is estimated that 226,650 people will be diagnosed with lung cancer and 124,730 will die from the disease in the United States, making it the most common cause of cancer death. While early-stage lung cancer is highly curable, most patients are diagnosed at advanced stages, resulting in poor survival rates.

Low-dose CT scans can detect lung cancer early, significantly reducing mortality, as shown in the National Lung Screening Trial. Based on this evidence, screening is recommended for high-risk individuals, but screening uptake remains low.

“Recent advancements in lung cancer screening reduces mortality by 20% to 30% by identifying cancer in its early stages,” said Robert Van Haren, MD, MSPH, Cancer Center member and associate professor at the University of Cincinnati College of Medicine. “A significant gap remains between screening eligibility and uptake for lung cancer. This project will identify UC Health primary care clinics with strong screening performance and use physician and patient focus groups to better understand the barriers that prevent screening and the strategies that lead to success.”

Van Haren and his team are committed to understanding why this gap between eligibility and uptake exists across the UC Health system. The central hypothesis is that specific clinic- and patient-level factors contribute to this issue, and identifying these differences can lead to targeted, system-wide improvements.

“Our first objective is to use electronic health records to compare factors such as patient demographics, clinic size, location and provider ratios to determine what differentiates high-utilization clinics,” he explained. “Our second objective it to conduct focus groups with providers, staff and patients to explore cultural and systemic factors that influence screening, including barriers and successful practices.”

This innovative, team-based study combines data analytics with firsthand perspectives to design practical, clinic-level interventions. By focusing on real-world workflows and engaging the full healthcare team, the project aims to create scalable solutions that can enhance screening practices and ultimately improve early detection and outcomes for lung cancer patients.

Genome-Scale Characterization of the Human Response to Human Papillomavirus Infection in Head/Neck Cancers

Matthew Weirauch, PhD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center Researcher, Divisions of Human Genetics, Biomedical Informatics, and Developmental Biology Cincinnati Children’s Hospital Medical Center

“It is well established that human papillomavirus (HPV) plays a direct role in the development of several cancers, though the underlying mechanisms are not fully understood,” said Matthew Weirauch, PhD, Cancer Center member and researcher at Cincinnati Children’s Hospital Medical Center. “This project focuses on understanding what is happening on a molecular level.”

HPV, or human papillomavirus, is a group of over 200 related viruses, some of which are spread through vaginal, anal or oral sex. Sexually transmitted HPV types fall into two groups: low risk and high risk. High-risk HPVs can cause several types of cancer. There are twelve high-risk HPV types — HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59 — but HPV 16 and HPV 18 are responsible for most HPV-related cancers.

Weirauch and his team aim to uncover how HPV alters host cell function to increase the risk of head and neck squamous cell carcinomas (HNSCCs), particularly those associated with high-risk HPV types 16, 18 and 31. Using genome-scale techniques, the team will characterize changes in gene expression, chromatin accessibility and transcription factor activity.

“Viruses, such as HPV, are likely involved in many chronic human diseases, but we still do not understand how,” Weirauch shared. “Virus infection has a huge effect on human cells, causing upwards of thousands of changes to human gene expression levels and tens of thousands of epigenetic changes. Modern genome-scale experimental and computational approaches allow us to study this problem in ways we never could before. Our work is systematically linking the effects of a range of viruses to a range of chromic human diseases and cancers.”

While his earlier work focused on autoimmune diseases, Weirauch is building on his foundational expertise in gene regulation and leveraging advanced genomic technologies to explore how viral infections disrupt cellular function and contribute to cancer development.

“With a background in bioinformatics, functional genomics and gene regulation, I’ve primarily focused on autoimmune diseases,” he said. “Joining the Cancer Center has allowed me to apply this expertise to oncology research. Because gene regulation operates through universal mechanisms, the tools and techniques I've developed can be readily adapted to understand cancer-related pathways.”

Elucidating the Role of Acid Sphingomyelinase Expression in Pancreatic Ductal Adenocarcinoma

Gregory Wilson, MD Associate Member, Experimental Therapeutics Research Program University of Cincinnati Cancer Center Assistant Professor, Department of Surgery University of Cincinnati College of Medicine

Accounting for more than 80% of pancreatic cancer, pancreatic ductal adenocarcinoma, which begins in the cells of the pancreas’ ducts that transport juices containing digestive enzymes to the small intestine, is the most common form of pancreatic cancer. Additionally, pancreatic cancer is the fourth most common cause of global cancer-related deaths and is almost always fatal.

“Pancreatic ductal adenocarcinoma (PDAC) continues to have some of the poorest treatment outcomes among all cancers, underscoring the urgent need to uncover new molecular drivers and therapeutic strategies,” said Gregory Wilson, MD, associate member of the Cancer Center and assistant professor at the University of Cincinnati College of Medicine. “Emerging evidence links acid sphingomyelinase (ASM) expression with patient survival in PDAC. This project will explore a novel pathway by which ASM contributes to PDAC development and progression, potentially offering a new therapeutic angle.”

Acid sphingomyelinase (ASM) is an enzyme that breaks down sphingomyelin into ceramide and phosphorylcholine, and it plays a crucial role in cell signaling, stress responses and even cell death. In pancreatic ductal adenocarcinoma, high expression of ASM correlates with improved long-term survival and may contribute to a better response to neoadjuvant therapy, meaning that low expression of ASM is associated with poorer prognosis.

“We believe that molecules released by tumors, called polyamines, reduce ASM activity, causing a buildup of fats (sphingomyelin) in cell structures called lysosomes,” Wilson explained. “This buildup weakens the immune system through a chain reaction involving TFEB signaling, leading to lower arginine levels — an important nutrient for immune cells. As a result, the body’s ability to fight the tumor is reduced. Early results suggest that giving back ASM through a treatment could block this process and offer a new way to treat pancreatic cancer.”

Determinants of Delay in EGFR Inhibitor Initiation and Its Impact on Clinical Outcomes in Non-Small Cell Lung Cancer Patients

Xiaomo (Shawn) Xiong, PhD Associate Member, Cancer Prevention, Control & Population Sciences Research Program University of Cincinnati Cancer Center Assistant Professor, Division of Pharmacy Practice & Administrative Sciences University of Cincinnati College of Pharmacy

In 2025, it is estimated that 226,650 people will be diagnosed with lung cancer and 124,730 will die from the disease in the United States, making it the most common cause of cancer death. There are two main types of lung cancer — small cell lung cancer and non-small cell lung cancer.

“Non-small cell lung cancer (NSCLC) is the most prevalent subtype of lung cancer,” said Xiaomo (Shawn) Xiong, PhD, associate member of the Cancer Center and assistant professor at the University of Cincinnati College of Medicine. “EGFR tyrosine kinase inhibitors (TKIs) are a key treatment for NSCLC, but they only work if the cancer has certain mutations. This makes early testing for EGFR mutations critical, yet delays can happen for many reasons — how the test is done, a patient’s overall health or even where they receive care. These delays may affect how well patients respond to treatment.”

EGFR tyrosine kinase inhibitors (TKIs) are a class of drugs that block the epidermal growth factor receptor (EGFR) — a protein on the surface of some cells that helps control how they grow and divide. When EGFR is too active, especially on cancer cells, it can lead to uncontrolled growth. EGFR TKIs inhibit this pathway and, therefore, can slow or stop cancer development. However, their effectiveness depends on identifying EGFR mutations through genetic testing. Despite the importance of early testing, logistical and clinical barriers often delay timely assessment and treatment initiation.

“This study aims to uncover the factors contributing to delays in the initiation of EGFR-targeted treatments following genetic testing in patients with NSCLC and to evaluate how such delays affect outcomes including survival and healthcare utilization,” shared Xiong. “The broader significance lies in enhancing the implementation of precision oncology by ensuring not only the development of effective therapies, but also their timely delivery.”

By focusing on the timing between biomarker testing and treatment initiation, the research highlights a crucial and often overlooked step in the delivery of precision oncology. While the clinical benefits of EGFR-targeted therapies are well-established, gaps in timely implementation may compromise patient outcomes. Through this study, Xiong and his team aim to generate actionable insights that can inform pharmacist-led and system-level interventions to streamline biomarker-based care.

“Our study will bridge a critical gap between biomarker testing and treatment implementation,” he said. “Receiving this award is not only a meaningful milestone in my early career, but it also validates the importance of addressing real-world barriers in precision oncology. This support enables us to generate impactful evidence on how to improve timely access to EGFR-targeted therapies. It also empowers me to advance equity-driven, data-informed cancer care and build a stronger foundation for future NIH- and NCI-funded research.”

As an early-career investigator, Xiong credits the spirit of team science fostered by the Cancer Center as essential contributors to the success of his work. His access to multidisciplinary collaborators has strengthened the study’s design and execution, and the supportive environment has not only accelerated his growth as a researcher but also provided the infrastructure needed to pursue meaningful, patient-centered questions in precision oncology.

“My Cancer Center membership has provided critical resources, from biostatistics support to a collaborative network of oncologists and pharmacists, which really shaped this study's design and execution,” he shared. “Importantly, the Cancer Center’s Pilot Project Award Program has enabled us to pursue real-world questions that truly matter for patient care and health equity. This environment has been foundational in launching a research program focused on improving precision oncology delivery.”

Cytoskeletal Dynamics and ECM Remodeling in the Melanoma Microenvironment

Yuhang Zhang, PhD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center Professor, Department of Dermatology University of Cincinnati College of Medicine

While recent therapies have made strides in improving early outcomes for melanoma patients, the challenge of drug resistance remains a major barrier to sustained treatment success. Cancer-associated fibroblasts play a key role in this by influencing how tumors respond to treatment.

Cancer-associated fibroblasts (CAFs) are a type of stromal cell that play a crucial role in the tumor microenvironment by interacting with cancer cells and the extracellular matrix (ECM). CAFs, along with other stromal cells and the ECM, contribute to tumor progression, invasion and metastasis by altering ECM structure, facilitating cell migration and influencing immune responses.

“My lab focuses on understanding a major stromal cell population in melanoma known as cancer-associated fibroblasts (CAFs),” shared Yuhang Zhang, PhD, Cancer Center member and professor at the University of Cincinnati College of Medicine. “Therapeutic agents often cause unexpected effects on stromal cells, which then contribute to cancer resistance and recurrence. Our work aims to identify druggable targets in CAFs to eliminate tumor stroma-induced drug resistance in melanoma cells for improved patient outcomes.”

Building on the recognition that stromal cells play a critical role in cancer resistance, Dr. Zhang’s research delves deeper into the complex interactions between cancer-associated fibroblasts and targeted therapies.

“Understanding how cancer-associated fibroblasts (CAFs) are regulated and how they respond to treatment is essential for improving therapeutic outcomes,” said Zhang. “This research focuses on identifying a master regulator of the response, regulation and reinforcement of CAFs in melanoma under targeted therapy. If successful, there is an opportunity to design a treatment strategy that targets CAFs to break the stromal barrier and improve cancer therapy.”

Receiving this award marks a crucial step forward for Zhang and his team. With the support from the Pilot Project Award Program as well as the Cancer Center overall, they can carry out key experiments and gather the data necessary for a forthcoming grant application to the National Cancer Institute.

“This award will allow us to perform essential experiments and collect the data needed for a new grant application that will be submitted to the National Cancer Institute in the near future,” he said. “The Cancer Center has been instrumental in supporting our research by offering funding for both our main projects and preliminary studies as well as providing access to a wide range of core facilities essential for this research. Additionally, the quarterly seminar series and annual retreat create dynamic environments for problem-solving and idea exchange, which greatly contribute to the growth and progression of our research efforts.”