The University of Cincinnati Cancer Center Pilot Project Award Program is dedicated to advancing cancer research by providing pilot funding to faculty investigators. The goals of this program 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.

Eight Cancer Center members received funding for their pilot projects in the 2026 Spring cycle. Congratulations to all the awardees!

Targeting TXNRD1 Overcomes Resistance to RAS Inhibition in Lung Cancer

Cristina Andreani, PhD Associate Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center

Lung cancer remains the leading cause of cancer-related mortality worldwide, responsible for over 1.8 million deaths annually and accounting for about 18% of all cancer deaths. While therapeutic advances have improved outcomes, intrinsic and acquired resistance continue to limit durable clinical responses.

“Targeted therapies against KRAS, one of the most altered genes in lung cancer, have transformed patient care,” said Cristina Andreani, PhD, an associate member of the Signaling Networks & Metabolic Pathways Research Program at the Cancer Center. “Unfortunately, most tumors eventually become resistant and begin growing again. Our research focuses on understanding why this happens.”

Andreani and her team study a small population of cancer cells known as drug-tolerant persister (DTP) cells—a small subpopulation of cells that survive treatment through reversible, non-genetic adaptations. By entering a slow-growing or dormant state, they endure treatment and cause relapse after the drugs are withdrawn.

“We recently discovered that these DTP cells become highly dependent on a protein called Thioredoxin Reductase 1 (TXNRD1), which helps them manage oxidative stress and survive therapy,” Andreani explained. “By blocking TXNRD1, we can trigger ferroptosis—a form of cell death caused by overwhelming lipid oxidation—selectively killing these resistant cells. Our goal is to determine whether combining KRAS-targeted therapies with TXNRD1 inhibition can eliminate these DTP cells and prevent tumor relapse.”

By integrating advanced spatial transcriptomic and lipidomic technologies, the research will also define the molecular mechanisms that enable these cells to survive treatment. Addressing one of the most significant challenges in oncology—therapy resistance—the work examines the non-genetic adaptations that allow cancer cells to persist, rather than focusing solely on treatment-induced genetic mutations. The findings may establish a new therapeutic strategy for preventing relapse in KRAS-driven lung cancer and could have broader implications for overcoming resistance in other cancers treated with targeted therapies.

Support from this award will provide critical resources to investigate TXNRD1-targeted therapeutic strategies in clinically relevant preclinical models and to implement advanced spatial multi-omic approaches to study mechanisms of therapy resistance. Additionally, by expanding collaborations with experts in computational biology, spatial transcriptomics and thoracic oncology, the project will help accelerate the translation of these discoveries into future clinical studies.

“My laboratory studies how cancer cells adapt their metabolism and redox balance to survive targeted therapies, with the long-term goal of identifying vulnerabilities that can be therapeutically exploited,” Andreani shared. “Support from this award will allow us to generate critical preclinical data, develop new collaborations in spatial multi-omics and accelerate the translation of our discoveries toward improved treatments for patients with lung cancer. It will also provide an important foundation for future NIH-funded studies and help establish my laboratory as a leader in the field of redox biology and therapy resistance.”

Andreani noted that the collaborative and resource-rich environment of the Cancer Center has been instrumental in supporting this work and advancing the translational direction of her research. She emphasized that access to specialized technologies, multidisciplinary expertise and institutional pilot funding programs has helped position her laboratory to pursue innovative approaches to therapy resistance in lung cancer.

“My Cancer Center membership has played a critical role in the development of my research program and career progression,” she said. “The Cancer Center provides access to exceptional shared resources, including genomics, lipidomics, metabolomics, bioinformatics, pathology and preclinical modeling cores, which have significantly strengthened the rigor and scope of my work. Just as importantly, the collaborative environment has connected me with basic scientists, computational biologists, clinicians and patient advocates whose expertise has enhanced the translational relevance of my research.”

Targeted mRNA Delivery to Reprogram T Cells and Sensitize HNSCC Tumors to Immune Checkpoint Inhibitors

Ameet A. Chimote, PhD, MS, MBBS Associate Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center

Affecting approximately 66,000 Americans each year, head and neck squamous cell carcinoma (HNSCC) is the most common histologic type of head and neck cancer. HNSCC is an aggressive malignancy that originates in the squamous epithelial cells of the mucosal linings within the head and neck region, such as the oral cavity, pharynx, and nasal cavity. These tumors are often highly invasive and have the potential to metastasize to regional and distant tissues, making them notoriously difficult to treat.

While checkpoint inhibitor immunotherapies, such as pembrolizumab, are available for HNSCC patients, most do not respond to treatment. A major contributor to this resistance is the tumor’s ability to suppress critical potassium ion channels in T cells, impairing their capacity to mount an effective antitumor immune response.

“Our laboratory has studied this mechanism, which we term “ionic checkpoint suppression,” for more than a decade,” shared Ameet A. Chimote, PhD, MS, MBBS, an associate member of the Signaling Networks & Metabolic Pathways Research Program at the Cancer Center. “Building on this work, we developed specialized lipid nanoparticles designed to deliver genetic instructions directly to T cells in vivo and restore the activity of these critical ion channels. In preliminary studies, this nanoparticle-based therapy reduced tumor burden by approximately 70% in head and neck cancer models.”

Through this project, Chimote and his team will determine whether combining this nanoparticle therapy with currently approved immunotherapies further improves antitumor responses using three complementary models: a patient-derived tumor-on-a-chip system with autologous immune cells, a humanized mouse model, and an immunocompetent syngeneic mouse model. Together, these models will provide important insight into the translational potential of this therapeutic strategy.

“If successful, this study will establish a strong preclinical foundation for a new class of cancer immunotherapy that restores intrinsic immune cell function by reactivating key molecular machinery, rather than inhibiting external checkpoint pathways,” he said. “This approach could expand effective treatment options to the majority of patients with head and neck cancer who currently do not benefit from approved immunotherapies.”

After more than a decade in the laboratory of Laura Conforti, PhD—first as a postdoctoral fellow and later as a research scientist—Chimote recently established his own independent laboratory, making this award particularly meaningful.

“This award is especially significant to me at this point in my career as I recently established my own independent laboratory thanks to Dr. Conforti’s mentorship, scientific guidance and unwavering support, which have been instrumental in this transition,” he said.

Launching an independent laboratory requires substantial resources, momentum and institutional support, all of which are aided by this Pilot Project Award.

“This funding will support key multi-model preclinical studies to establish proof-of-concept for our nanoparticle immunotherapy platform and directly strengthen a planned R01 application to the National Cancer Institute,” said Chimote. “As a physician-scientist who completed medical training in India and subsequently pursued advanced research training in the United States, this recognition from the University of Cincinnati Cancer Center represents a meaningful and deeply valued milestone in my career.”

Chimote also emphasized that this award not only supports the immediate goals of establishing proof-of-concept data for his nanoparticle immunotherapy platform, but also represents an important step in his broader integration into the University of Cincinnati Cancer Center research community.

“After joining the Cancer Center in May, this Pilot Project Award marks the first instance of direct research support from the Cancer Center,” he said. “As I continue to build my laboratory, I look forward to utilizing the full breadth of Cancer Center resources, including the Biospecimen Shared Resource, the collaborative scientific network and the translational research infrastructure. This award demonstrates the tangible impact of Cancer Center membership for early-stage investigators and highlights the opportunities that this affiliation will provide in supporting future growth.”

Co-Designing Nutrition-Based Graphic-Style Stories with Adults with Intellectual and Developmental Disabilities and Their Caregivers for a Community Cancer Prevention Program

Laura Nabors, PhD, ABPP, CPH Associate Member, Experimental Therapeutics Research Program University of Cincinnati Cancer Center

Adults with intellectual and developmental disabilities (IDD) are more likely to experience overweight and obesity than the general population, placing them at an increased risk for chronic diseases, including certain cancers. Despite this elevated risk, many individuals with IDD and their caregivers lack awareness of the connection between diet and cancer prevention, and there are few tailored educational programs addressing this gap. Additionally, caregivers—including family members, guardians, and community program staff—lack structured guidance on how to effectively communicate nutrition and health information.

Laura Nabors, PhD, ABPP, CPH, an associate member of the Experimental Therapeutics Research Program at the Cancer Center, is a part of a team working to address this gap by developing and testing a co-designed, nutrition-focused cancer prevention education program for adults with IDD and their caregivers. Using an iterative community co-design process developed by We-Engage-4-Health and led by Melinda Butsch Kovacic, PhD, MPH, Associate Director for Community Outreach and Engagement at the Cancer Cetner, adults with IDD, caregivers, staff, and researchers will collaboratively create engaging graphic-style stories and supporting activities.

“This project is unique in its use of a peer-informed co-design approach in which adults with intellectual and developmental disabilities contribute directly to the development of health education materials for their own community and caregivers,” she explained. “It will generate new knowledge on the use of participatory co-design methods to create video-based educational stories that link healthy eating with cancer risk reduction, with materials designed to remain accessible to participants for ongoing use.”

Nabors’ research addresses a critical need for cancer prevention and nutrition education in a population at an increased risk for obesity, cardiovascular disease and cancer. Simultaneously, her research also advances the Cancer Center’s community outreach and engagement mission. More broadly, this project will contribute evidence on how to co-develop effective, user-centered educational interventions for this population and lay the foundation for future proposals from the research team.

The research team—Laura Nabors, PhD, ABPP, CPH; Melinda Butsch Kovacic, PhD, MPH; and Seung-Yeon Lee, PhD, an associate member of the Population Science & Cancer Control Research Program at the Cancer Center—is well-positioned to carry out this work, with extensive experience in community engagement and the development of graphic-style nutrition education materials for underserved populations.

We Engage 4 Health and Butsch Kovacic have already produced more than 80 stories, including cancer-focused content, many of which have been compiled into a published educational resource. The team also brings established partnerships with adult day programs and prior experience developing and evaluating nutrition interventions for adults with IDD, including the Eat and Exercise to Win program.

Additionally, the team will be partnering with Marjorie Book Continuing Education—a Cincinnati-based nonprofit that brings together adolescents and adults both with and without disabilities for inclusive, community-driven programs—and Joseph Link, an associate professor in the Special Education Program at the University of Cincinnati College of Education, Criminal Justice and Human Services.

Building on this strong foundation of community partnerships, established educational resources and prior intervention work, Nabors emphasized the significance of this award in advancing their shared goals. She further underscored the project’s scientific relevance and personal meaning in addition to the broader impact of Cancer Center membership on her research trajectory and professional growth.

“This award is especially meaningful to me because it allows me to support adults with intellectual and developmental disabilities in learning how to reduce cancer risk through practical health behaviors designed through a co-development process with their community,” she said. “This work reflects the goals I have long aspired to achieve, and I am truly grateful for this opportunity. Additionally, my Cancer Center membership has been tremendously impactful as I have gained substantial insight and guidance through the Cancer Center’s programming as well as the mentorship by Dr. Butsch Kovacic. I am truly grateful to have the Cancer Center’s support.”

Mechanisms and Therapeutic Targeting of Pancreatic Cancer Growth and Metastasis Driven by a Novel Tumor Suppressor

Krushna C. Patra, PhD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center

Pancreatic ductal adenocarcinoma (PDA) is the most common and aggressive type of pancreatic cancer, accounting for over 90% of cases. Characterized by a dense, fibrotic tumor microenvironment (desmoplasia) and a high metastatic potential, it is a highly lethal disease often diagnosed at advanced stages, resulting in low overall survival rates.

“Pancreatic cancer remains one of the most difficult cancers to treat because it is often diagnosed after it has spread beyond the pancreas,” said Krushna C. Patra, PhD, a member of the Signaling Networks & Metabolic Pathways Research Program. “Understanding how cancer cells acquire the ability to spread is essential for developing more effective treatments.”

Patra’s laboratory studies how genetic alterations and cellular signaling pathways drive pancreatic cancer progression, with a focus on understanding the biological mechanisms that normally keep tumor growth and spread in check. His latest project builds on this work by examining how disruptions in these pathways allow cancer cells to become more aggressive.

Working alongside co-investigator Andrew Volk, PhD, Patra will focus on Salt-Inducible Kinases (SIKs), a group of proteins that help regulate cellular signaling and gene activity. Their research seeks to better understand how the loss of SIK signaling reshapes the gene programs that support tumor growth and metastasis.

“Cancer cells acquire the ability to invade surrounding tissues and establish tumors in distant organs through complex changes in gene regulation,” Patra explained. “Our work seeks to uncover the molecular events that contribute to this process and determine whether key components of these pathways can be targeted therapeutically.”

The project will also explore downstream signaling pathways that may serve as promising therapeutic targets, with the goal of identifying vulnerabilities that could be leveraged for future treatments. Because alterations in these pathways have been observed in multiple cancer types, the findings may have implications beyond pancreatic cancer.

For Patra, the support from the University of Cincinnati Cancer Center is especially meaningful as it allows his team to pursue bold, emerging ideas and generate the foundational data needed for larger-scale federal funding opportunities.

“This award comes at an important stage for our lab,” Patra said. “It allows us to refine our hypotheses, strengthen the project through early studies and move this work closer to larger NCI funding support.”

Together, these studies aim to uncover key mechanisms that drive pancreatic cancer progression and lay the groundwork for new therapeutic strategies to improve outcomes for patients facing this devastating disease.

Bridging the Screening Gap: A Pilot Study of Primary HPV Self-Collection within an Emergency Department Early Intervention Program (BeSCRN'D)

Leeya F. Pinder, MD, MPH Member, Population Science & Cancer Control Research Program University of Cincinnati Cancer Center

Cervical cancer remains a significant public health challenge, particularly in underserved populations where disparities in incidence and mortality persist despite the availability of effective screening. Ohio faces alarming inequities in outcomes with Black women in the state experiencing a 36% higher death rate from cervical cancer compared to White women.

“We know that the gap in cervical cancer outcomes is deeply rooted in systemic inequities that disproportionately burden Black and Latino populations, which directly hinder timely screening and preventive intervention,” said Leeya F. Pinder, MD, MPH, Interim Associate Director for Population Science & Cancer Control at the Cancer Center. “These challenges are further intensified for highly vulnerable populations, such as individuals experiencing homelessness or those contending with substance use disorders, who face unique obstacles to regular healthcare engagement. Furthermore, Ohio's low HPV vaccination rates—with less than 50% of eligible girls completing the series—highlight a critical gap in primary prevention that necessitates innovative, low-barrier secondary prevention strategies.”

The Emergency Department (ED) serves as an important point of healthcare access for many underserved populations who may not regularly engage with primary care services. Literature suggests that up to 50% of ED visits are "primary care eligible," indicating that the ED often functions as the only point of contact for non-emergent health concerns among underserved groups.

“At UC Health, the ED sees approximately 60,000 patient visits annually, with many patients relying on government insurance or self-pay options, underscoring the ED’s role as a critical safety-net setting,” shared Pinder. “A substantial proportion of visits involve adults within the recommended cervical cancer screening age range, providing an important opportunity to reach individuals who might otherwise miss preventive care.”

BeSCRN'D is designed to evaluate the strategic integration of cervical cancer prevention into the established Early Intervention Program (EIP) already operating within the Emergency Department (ED) at UC Health. Founded in 1998 to provide HIV education and screening, the EIP has extensive experience serving marginalized and stigmatized populations through culturally responsive, patient-centered care.

“The EIP’s success is built upon a highly skilled team of Health Promotion Advocates and Linkage Coordinators trained in motivational interviewing and client-centered counseling,” Pinder explained. “In 2026, the EIP team risk-assessed 4,024 patients, demonstrating the high-volume capacity of this existing platform. By embedding cervical cancer screening within this trusted infrastructure, the health system can offer preventive services without the need for additional appointments, directly addressing the logistical and trust-based barriers that impede screening in traditional settings.”

A key innovation of the BeSCRN’D project is the use of primary high-risk HPV self-collection (pHPVsc), recently approved by the FDA as a patient-centered cervical cancer screening approach.

“Studies have shown that self-collected HPV testing performs similarly to clinician-collected samples while reducing many of the barriers associated with pelvic exams, including discomfort, stigma, anxiety and logistical challenges,” Pinder said. “Self-collection has also been associated with improved screening participation among underserved populations.”

While pHPVsc offers a promising solution to bridge the screening gap, real-world implementation data is urgently needed to understand how to effectively integrate this tool into high-intensity safety-net workflows like the EIP. The BeSCRN'D project will evaluate the feasibility, acceptability and appropriateness of integrating pHPVsc into the EIP workflow.

“Guided by the RE-AIM and Levesque frameworks, the project will generate implementation data needed to support future large-scale NIH and NCI proposals,” Pinder shared. “My co-investigators—Caroline E. Freiermuth, MD; Shanna D. Stryker, MD, MPH; and Lucrecia Mena-Meléndez, PhD, MA—and I are dedicated to developing evidence-based approaches to improve access to cancer prevention services. Our goal is to show that integrating accessible cervical cancer screening into trusted healthcare settings can help close longstanding gaps in prevention, improve patient trust and engagement, and expand care for communities disproportionately impacted by healthcare inequities.”

The Lands Cycle as a Ferroptosis‑Suppressive Vulnerability in Mutant KRAS Lung Cancer

Pier Paolo P. Scaglioni, MD Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center

KRAS is a well-known gene that acts as an “on/off switch” for cell growth and division, sending signals to help healthy cells grow, divide and self-destruct when needed. When mutated, KRAS essentially gets stuck in the “on” position, causing cells to multiply uncontrollably. These mutations are a primary driver in many deadly cancers, underlying about 20% of all human malignancies.

“In lung cancer, mutant KRAS is not only sufficient to initiate tumor formation but is also required to maintain tumor survival, making it a high-priority therapeutic target,” said Pier Paolo P. Scaglioni, MD, Associate Director for Translational Research at the Cancer Center.

While highly selective KRAS inhibitors have recently been developed, resistance to therapy remains inevitable, and current chemotherapy and immunotherapy approaches benefit only a subset of patients. Therefore, there is a critical need to identify additional vulnerabilities in mutant KRAS-driven cancers.

“Our research has shown that mutant KRAS lung cancer depends on specific metabolic pathways, including fatty acid (FA) metabolism, for survival,” Scaglioni shared. “These findings have supported several early-phase clinical trials targeting metabolic pathways in mutant KRAS lung cancer, including studies evaluating inhibition of fatty acid synthase (FASN).”

Fatty acid metabolism includes the cellular pathways responsible for producing and breaking down fatty acids, which are essential for energy production, membrane structure and cell signaling. A key component of this process is fatty acid synthase (FASN), which drives de novo lipogenesis, the synthesis of new fatty acids from simple molecular precursors. In mutant KRAS cancers, oncogenic signaling rewires cellular metabolism and increases production of reactive oxygen species (ROS). Without adequate antioxidant and lipid repair mechanisms, these ROS can damage cellular membranes through lipid peroxidation. Although lipids are known to play critical roles in membrane integrity, signaling, and energy metabolism, their contribution to regulating ferroptosis and other cell death pathways remains incompletely understood.

“Our previous studies demonstrated that mutant KRAS stimulates de novo fatty acid synthesis and that inhibition of fatty acid synthase (FASN) induces ferroptosis in mutant KRAS lung cancer models,” Scaglioni explained. “Ferroptosis is an iron-dependent form of regulated cell death driven by the accumulation of oxidized phospholipids. These findings suggest that fatty acid metabolism is not simply required for basic cell function but instead represents a cancer-specific survival mechanism.”

Most ferroptosis research has focused on antioxidant defense systems that control oxidative stress, while much less is known about the lipid repair pathways that protect cancer cells from membrane damage. One important repair pathway is the Lands cycle, which maintains membrane integrity by removing and replacing damaged fatty acid chains within phospholipids.

“The Lands cycle depends on two major enzyme groups: phospholipase A2 (PLA2) enzymes, which remove damaged fatty acids from phospholipids, and lysophospholipid acyltransferases (LPLATs), which restore repaired phospholipids,” said Scaglioni. “Using expression profiling and targeted siRNA screening, our preliminary studies identified PLA2G4C and LPCAT3 as key Lands cycle enzymes in mutant KRAS lung cancer. These enzymes appear to direct newly synthesized fatty acids toward membrane repair, preventing the buildup of oxidized phospholipids that would otherwise trigger ferroptosis.”

Together, these findings suggest that mutant KRAS lung cancer cells depend on the Lands cycle to preserve membrane integrity, avoid ferroptotic cell death, and maintain tumor survival. This proposal will test that hypothesis using mass spectrometry, functional assays, lung cancer cell models and mouse tumor models to determine whether the Lands cycle represents a targetable metabolic vulnerability in mutant KRAS lung cancer.

Scaglioni noted that this project builds on the Cancer Center’s collaborative and translational research environment, which has provided critical infrastructure and scientific partnerships to support the study’s development.

“Cancer Center membership has been instrumental in advancing this research by providing access to critical shared resources while also fostering collaborations with experts in cancer metabolism, lipid biology and translational science,” he shared. “The Cancer Center’s pilot funding programs have created opportunities to pursue innovative, high-risk ideas, and the interdisciplinary research environment has greatly strengthened the rigor, creativity and translational impact of this work.”

STAT-VEN-AZA: PitavaSTATin Added to VENetoclax and AZAcitidine for TP53 Mutated Acute Myeloid Leukemia

Sarah J. Skuli, PhD Associate Member, Signaling Networks & Metabolic Pathways Research Program University of Cincinnati Cancer Center

Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow. It occurs when the bone marrow produces abnormal, immature white blood cells that multiply rapidly and crowd out healthy red blood cells, white blood cells and platelets. Each year, AML affects over 20,000 people in the United States and has an overall five-year survival rate of only about 30%.

“Acute myeloid leukemia (AML) is an aggressive blood cancer,” said Sarah J. Skuli, MD, PhD, an associate member of the Signaling Networks & Metabolic Pathways Research Program at the Cancer Center. “Patients whose leukemia contains mutations in the TP53 gene have particularly poor outcomes even with the current advances we've made in AML treatment.”

The TP53 gene is a vital tumor suppressor gene often referred to as the "guardian of the genome." Located on chromosome 17p13.1, it produces the p53 protein, which regulates cell division, repairs damaged DNA and forces severely damaged cells to die, also known as apoptosis. When mutated, TP53 fails to repair cellular DNA or kill off mutated cells, leading to uninhibited tumor growth and is the most common genetic alteration in human cancers.

Acute myeloid leukemia with TP53 mutations is one of the most aggressive and treatment-resistant subtypes of leukemia. It accounts for 5–10% of de novo AML cases and is frequently associated with complex chromosomal abnormalities and a very poor prognosis, yielding a median survival of only five to ten months.

“TP53 mutations are especially common in therapy-related and secondary AML, which often arise after prior chemotherapy or radiation exposure,” Skuli shared. “As survival improves for other cancers, the incidence of TP53 mutant AML is expected to increase, highlighting the urgent need for more effective treatment approaches.”

Current treatment options for acute myeloid leukemia with TP53 mutations remain limited and enrollment in clinical trials is often recommended as first-line therapy. However, few promising therapeutic strategies are currently in advanced clinical development.

“My research focuses on understanding the biology and treatment resistance mechanisms of TP53 mutant AML,” said Skuli. “We previously identified increased activation of the cholesterol synthesis pathway as a key feature distinguishing TP53 mutant AML from TP53 wild-type AML. Importantly, this pathway becomes further activated in response to therapy, suggesting that cholesterol metabolism contributes to treatment resistance.”

Building on these findings, Skuli and her team demonstrated that statins—a widely used class of FDA-approved cholesterol-lowering medications—can sensitize TP53 mutant AML cells to standard therapies, including venetoclax and azacitidine. These results identify the cholesterol synthesis pathway as a novel therapeutic target in TP53 mutant AML.

“To further investigate the clinical relevance of these findings, we performed a multi-center retrospective study evaluating outcomes in newly diagnosed TP53 mutant AML patients who were taking statins at diagnosis,” Skuli explained. “Patients who discontinued statins had significantly worse survival compared to those who continued statin therapy or had never received a statin. These findings suggest that statins are generally safe in AML patients and may provide clinical benefit.”

Previous studies evaluating statins in acute myeloid leukemia (AML) have produced mixed results, likely because they did not focus specifically on high-risk AML subtypes, such as acute myeloid leukemia with TP53 mutations. Skuli and her team’s work suggests that the benefit of statins may be greatest in therapy-resistant AML cells, particularly those with TP53 mutations.

“Pitavastatin was selected for this study because it has several favorable properties for AML treatment,” said Skuli. “It is a lipophilic statin with good systemic availability, allowing it to directly target leukemia cells. Importantly, clinically achievable plasma levels overlap with concentrations shown to inhibit the cholesterol synthesis pathway in laboratory studies. Pitavastatin also has minimal interaction with cytochrome P450 3A4, reducing the risk of drug-drug interactions with AML therapies.”

Early clinical data suggest that pitavastatin can be safely combined with venetoclax-based therapy, but studies to date have included very few AML patients and none specifically with TP53 mutations. This study is designed to establish the safety, feasibility and biologic activity of pitavastatin in TP53 mutant AML and to support development of a larger efficacy-focused clinical trial.

Furthermore, this study reflects years of translational research focused on understanding treatment resistance in aggressive forms of leukemia and identifying strategies to improve outcomes for patients with limited therapeutic options. She noted that the project represents a meaningful opportunity to bridge laboratory discovery and patient-centered clinical research.

“For over 15 years, my academic and clinical training has centered on AML, from my undergraduate research at the University of Pennsylvania to my PhD studies at the University of Toulouse and medical training at Johns Hopkins University School of Medicine,” she shared. “Now, at the University of Cincinnati and the Cancer Center, I combine patient care with laboratory research focused on understanding and overcoming treatment resistance in leukemia. This award represents an important opportunity to move a promising therapeutic strategy from the laboratory to a clinical study for patients with one of the most aggressive and difficult-to-treat forms of AML.”

Skuli also took a moment to emphasize the important role the Cancer Center has played in supporting this project’s development and advancing its translational goals.

“My Cancer Center membership has been essential in advancing this research by providing access to collaborative expertise, shared core resources, clinical trial infrastructure and mentorship opportunities,” she said. “Through the Cancer Center, our team has been able to work closely with experts in biostatistics, translational science, clinical trial development and community engagement, all of which have strengthened the scientific and clinical foundation of this project. These collaborations have been critical in helping translate our laboratory discoveries into a clinical trial for patients with AML.”

Evaluating the Feasibility, Acceptability, and Preliminary Psychological Impact of Machine Learning-Matched, Therapist-Led Cognitive Behavioral Group Therapy for Adult Cancer Survivors Using the OncoSupport Platform

Anjanette A. Wells, PhD, LISW Associate Member, Population Science & Cancer Control Research Program University of Cincinnati Cancer Center

Advances in cancer screening, diagnosis and treatment have led to a rapidly growing population of cancer survivors in the United States. In 2022, over 18 million Americans were living with a history of cancer, and that number is expected to continue increasing over the coming decades. As survivorship care expands, there is growing need for long-term services that address not only physical health and treatment-related side effects but also psychological well-being.

“Psychological distress is one of the most common unmet needs among cancer survivors,” said Anjanette A. Wells, PhD, LISW, an associate member of the Population Science & Cancer Control Research Program at the Cancer Center. “Many individuals experience anxiety, depression, fatigue and fear of recurrence long after completing treatment, which can negatively affect recovery, quality of life, daily functioning and adherence to follow-up care.”

Although psychosocial interventions have been shown to improve emotional well-being and quality of life in cancer survivors, access to these services remains limited. Transportation challenges, scheduling barriers, shortages of psycho-oncology providers and uneven availability of survivorship services often prevent patients from receiving ongoing support, especially after active treatment ends.

“Group-based therapy offers one potential solution because it allows a single therapist to support multiple survivors at once,” Wells explained. “However, traditional cancer support groups are often made up of individuals with very different diagnoses, treatments, life experiences and emotional needs. This can reduce group connection and limit the perceived relevance of the discussions.”

Research has shown that group cohesion is one of the strongest predictors of successful outcomes in group psychotherapy, suggesting that more thoughtfully matched groups may improve engagement and benefit. Additionally, digital delivery can further improve access by allowing survivors to participate remotely. Studies have shown that virtual psychosocial interventions can improve anxiety, depression and quality of life while helping overcome geographic and mobility barriers.

“OncoSupport—a nonprofit and AI platform created by Siddhant Nagar, University of Cincinnati honors student in the medical sciences program—was developed to address these challenges by combining virtual therapist-led CBGT with personalized group formation,” Wells shared. “Rather than assigning participants based only on cancer diagnosis, the platform uses psychosocial and clinical factors—such as emotional distress, fear of recurrence, functional limitations, and life circumstances—to create more cohesive and supportive therapy groups. Preliminary analyses suggest this multidimensional matching approach produces stronger group cohesion than diagnosis-based grouping alone.”

This study will evaluate the feasibility, acceptability and preliminary psychological outcomes of OncoSupport among adult cancer survivors who completed primary treatment within the past year. Aim 1 will assess feasibility through recruitment, enrollment, retention, attendance, therapist fidelity and completion of outcome assessments, while also measuring participant satisfaction and usability. Aim 2 will evaluate preliminary changes in depression, anxiety, fear of recurrence, quality of life and group cohesion before and after the intervention.

The study will generate implementation data and preliminary outcome estimates needed to support a future multi-site randomized clinical trial and advance a scalable, personalized model of psychosocial survivorship care aligned with the mission of the Cancer Center.