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The University of Cincinnati Cancer Center is committed to developing the next generation of cancer researchers and providers. The Trainee Associate Membership Program offers trainees access to tools and resources to help them be productive and successful cancer researchers and professionals. Trainee Associate Members have access to a community of cancer trainees and mentors, pilot grants, seminar series and educational events, career development opportunities, and more. There are numerous benefits offered to Trainee Associate Members, including:
In the most recent cycle, nine Cancer Center Trainee Associate Members were selected for pilot project, travel and paper of the year awards. Congratulations to all the awardees!
Ahmet Kaynak, PhDTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Xiaoyang Qi, PhD
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, ranking fourth in cancer-related deaths in the United States and projected to rise to second by 2030. With a five-year mortality rate of approximately 94%, PDAC carries the worst prognosis among major malignancies. Because early symptoms are vague and reliable biomarkers are lacking, nearly 80% of patients are diagnosed with advanced, unresectable disease, including locally advanced or metastatic tumors.
“Given its aggressive nature, therapeutic resistance, and late-stage diagnosis, there is a critical need for novel treatment strategies,” said Ahmet Kaynak, PhD, trainee associate member of the Cancer Center. “Improved therapies will depend on a better understanding of the biological mechanisms that drive PDAC progression.”
A defining characteristic of malignant cell growth is the establishment of an immunosuppressive tumor microenvironment (TME). Within this environment, immunosuppressive M2 macrophages (MØs) promote tumor immune evasion and support continued tumor progression.
“We recently found that PDAC cells secrete a modified version of Hsp70 that drives M2 polarization and therefore promotes immune suppression,” shared Kaynak. “This differs from the normal intracellular version of the protein and appears to play a key role in generating immunosuppressive macrophages. The exact phosphorylation site responsible for this effect is still unknown.”
Heat shock protein 70 (Hsp70) is a highly conserved family of molecular chaperones that facilitate protein folding, stabilization, and degradation, primarily expressed in response to cellular stress. Typically, Hsp70 works inside healthy cells to aid other proteins fold properly and respond to stress. However, in pancreatic ductal adenocarcinoma (PDAC), the cells send this protein outside in a chemically modified form.
This modified version has a phosphate group attached to it — a change called phosphorylation. That small chemical change appears to make a big difference. Instead of performing its usual housekeeping role, the altered Hsp70 helps suppress the immune system.
Specifically, it encourages immune cells called macrophages to adopt an immunosuppressive state in which they do not attack the tumor and instead help protect it by dampening the body’s immune response. This allows the cancer to grow more easily and avoid being destroyed.
“In myeloid cells, neutralizing extracellular Hsp70 with a blocking antibody significantly reduced M2 polarization,” Kaynak said. “Furthermore, silencing Hsp70 expression in cancer cells decreased intratumoral M2 macrophage infiltration and slowed tumor growth.”
These findings demonstrate that tumor-secreted Hsp70 plays a direct role in shaping an immunosuppressive environment that supports cancer progression. However, while blocking or reducing Hsp70 clearly disrupted this process, the underlying molecular feature that enables Hsp70 to drive immune suppression remains unknown. Kaynak’s next step is to pinpoint the precise modification that gives the protein this tumor-promoting capability.
“With this award, my project aims to identify the specific phosphorylation site on Hsp70 that enables pancreatic cancer to suppress immune responses,” he said. “Defining this mechanism will uncover new ways PDAC evades immune surveillance and may identify precise molecular targets for therapeutic intervention.”
This research will provide new insight into how tumors manipulate immune cells at a molecular level. By identifying a specific, targetable modification of a cancer-secreted protein, Kaynak and his team can open the door to novel immunotherapeutic strategies, including antibody-based approaches designed to restore anti-tumor immunity.
Beyond its scientific impact, the project also represents an important milestone in Kaynak’s career development. The support will not only accelerate discovery in pancreatic cancer research but also help position him to build sustainable, independent research focused on tumor–immune interactions and therapeutic innovation.
“Receiving this TAM Award is an important step toward establishing my independent academic career,” he shared. “This award provides critical early-stage support that allows me to generate key preliminary data for a new project. These data will be essential for advancing the work and for pursuing future extramural funding, helping translate innovative ideas into impactful cancer research.”
Xiaoqin ZhuTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Andrew Volk, PhD
Acute myeloid leukemia (AML) is an aggressive blood cancer with poor long-term survival. It develops when immature myeloid cells fail to properly differentiate, leading to the buildup of leukemic blasts. Encouraging these cells to mature, or differentiate, offers a promising treatment strategy, but effective differentiation-based therapies for most AML cases are lacking.
“CHAF1B is part of the CAF-1 complex, which helps package newly replicated DNA into chromatin,” said Xiaoqin Zhu, trainee associate member of the Cancer Center. “Using proteomics, we identified HNRNPL as a new replication-associated partner of CHAF1B and confirmed their direct interaction. Although HNRNPL has been linked to cancer in solid tumors, its role in AML has not been defined.”
Heterogeneous nuclear ribonucleoprotein L (HNRNPL) is a crucial RNA-binding protein located in the nucleus that regulates alternative splicing, mRNA stability and translation. It plays a key role in cancer progression, specifically in prostate and lung cancer, by promoting proliferation, migration and survival.
“We discovered that HNRNPL is required to maintain AML cells in their leukemic state,” shared Zhu. “Removing HNRNPL forces these cells to differentiate and lose their ability to drive leukemia. Importantly, targeting HNRNPL does not appear to harm normal blood stem cells, suggesting a potential therapeutic window.”
Standard chemotherapy targets all rapidly dividing cells, which makes it effective but also non-selective, meaning that both cancer cells and healthy cells could be eliminated. This lack of specificity can allow some cancer cells to survive and relapse, while the loss of healthy cells can disrupt normal bodily functions, particularly in pediatric patients.
HNRNPL is best known as an alternative splicing factor, and Zhu and her team’s data indicate that it may also help prevent harmful transcription–replication conflicts. They propose that during DNA replication, CHAF1B recruits HNRNPL to regulate the splicing of genes that control cell fate and to suppress replication stress. This project aims to identify key downstream targets of this pathway and evaluate them as potential therapeutic opportunities in AML.
Beyond advancing the scientific understanding of AML, the project also plays an important role in Zhu’s professional development. The opportunity to lead this work not only accelerates progress toward identifying new therapeutic vulnerabilities but also supports her long-term goal of establishing an independent research program focused on cancer biology.
“Receiving this award represents a significant milestone in my career development, particularly as an international researcher building my academic path in the United States,” she shared. “The support would directly strengthen my training, enable completion of key research objectives and facilitate publication of high-impact manuscripts. In turn, this recognition would enhance my competitiveness for future postdoctoral opportunities and lay a strong foundation for establishing an independent research career in cancer biology.”
Megan BonesTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Linde Miles, PhD
Acute myeloid leukemia (AML) is an aggressive and molecularly complex malignancy characterized by the accumulation of cooperating genetic mutations that collectively impair myeloid differentiation. Despite advances in targeted therapies, the extensive genomic heterogeneity of AML fuels relapse and therapeutic resistance. Recent genomic studies have begun to reconstruct the underlying clonal hierarchies that drive disease development, revealing recurrent patterns of co-existing mutations in patient populations.
“My research investigates a clinically relevant subset of these mutations — IDH2, NPM1c and NRAS — with a particular focus on how activating NRAS mutations cooperate with IDH2 and NPM1c to drive leukemic transformation and reduce responsiveness to targeted inhibitors,” said Megan Bones, trainee associate member of the Cancer Center. “Our preliminary data suggest that the transition from a pre-leukemic to a leukemic state depends on sequential mutation acquisition, with each stage sustained by distinct cell-intrinsic programs and microenvironmental influences.”
Bones and her team have characterized aspects of the clonal architecture necessary for disease progression and begun exploring how these mutations functionally interact to determine clonal dominance and therapeutic response. In this project, they aim to define the complete clonal architecture of IDH2/NPM1c/NRAS-driven AML, elucidate the intrinsic mechanisms that maintain this state and uncover the molecular drivers of resistance to targeted treatments.
“This study would be one of the first studies to investigate the specific characteristics that NRAS mutations utilize to drive the leukemic state and promote resistance to targeted therapies,” Bones explained. “This project has the ability to discover new biology in the development of AML and will identify novel vulnerabilities in a subset of patients. Identifying these targetable vulnerabilities will allow for AML research in mutation specific resistance mechanisms to progress.”
Beyond its potential to uncover new therapeutic vulnerabilities in AML, the project also represents an important milestone in Bones’ scientific development. The opportunity to lead this work independently not only advances the field’s understanding of mutation-specific resistance mechanisms but also marks a significant step forward in her growth as a researcher.
“I am truly honored to receive this award as it marks my first independent source of funding during my doctoral training,” she shared. “This award and recognition validate the importance of this research direction and strengthens my confidence in its potential impact. Furthermore, the award provides critical resources to conduct in-depth mechanistic studies that will clarify how this clonal landscape is established and maintained.”
Reflecting on her development as a scientist, Bones credits the Cancer Center’s collaborative community and mentorship as key drivers of both her technical advancement and professional growth.
“Being part of the Cancer Center has significantly enriched my research and career trajectory,” she said. “The collaborative environment and resources have allowed me to refine my technical abilities while also developing key professional skills, including grant writing, scientific communication, and presentation. This support has empowered me to investigate fundamental questions about how AML arises, responds to therapy, and develops resistance.”
Presentation at the 2025 ASH Annual Meeting & Exposition
Junichiro Kida, MD, PhDTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Timothy Chlon, PhD
The DDX41 gene is a critical tumor suppressor gene that plays a key role in pre-mRNA splicing, RNA metabolism and innate immune sensing. Germline mutations in the DDX41 gene predispose individuals to myeloid malignancies, including myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), with approximately 50% of carriers developing disease by age 90.
“My research focuses on understanding the molecular mechanisms of myelodysplastic syndromes (MDS) and identifying novel therapeutic strategies,” said Junichiro Kida, PhD, trainee associate member of the Cancer Center. “Myelodysplastic syndromes (MDS) is a group of hematologic malignancies with poor prognosis, and our work centers on mutations in DDX41, the most common inherited cause of MDS. Among these, the p.R525H mutation is the most frequently observed, yet its functional role has remained poorly understood.”
Kida and his team discovered that p.R525H promotes differentiation into dendritic cells, which play an essential role in immune defense against infection and cancer. This suggests that disrupted dendritic cell development may play a role in disease progression.
“Most therapeutic strategies have focused primarily on targeting leukemic cells,” said Kida. “Our data suggest that the DDX41 p.R525H mutation also shapes the immune microenvironment, influencing surrounding immune cells and signaling molecules. We are currently examining how abnormal dendritic cells may promote leukemia by fostering a permissive immune setting. These insights could extend beyond DDX41-mutated disease to inform our understanding of blood cancers overall.”
As his work continues to uncover the role of the immune microenvironment in DDX41-mutated disease, the award not only underscores the importance of these findings but also supports the next phase of discovery.
“I am deeply honored to receive this award,” he said. “Being selected by leaders in the cancer research community affirms the significance of this work and reinforces my commitment to advancing this line of investigation. This award provides an invaluable opportunity to engage with colleagues at an international conference, fostering collaboration and expanding the reach of our findings.”
By connecting with investigators across disciplines and institutions, Kida sees the award as a catalyst — not only for scientific exchange, but also for advancing the long-term trajectory of the research and his career as he presents his work at the annual ASH Meeting & Exposition.
“Sharing our research on a global stage will help accelerate progress toward improved cancer therapies and prevention strategies while increasing the visibility of our team’s contributions,” he said. “Additionally, this recognition marks an important step in my professional development. It enhances my academic portfolio, broadens my professional network and strengthens my competitiveness for future extramural funding as I work toward establishing an independent research career.”
Kida also took a moment to credit the local research community at the Cancer Center with helping lay the groundwork for these broader opportunities.
“The Cancer Center’s resources have been invaluable to my research,” he shared. “In addition, the research-based events such as the annual Cancer Research Retreat and the annual Highlights of Hematology & Cellular Therapy Symposium provide excellent opportunities to connect with investigators, fostering collaborations that help drive innovative and impactful cancer research.”
Presentation at the 2025 Mid-Atlantic Gynecologic Oncology Society Annual Meeting
Rachel HillTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Leeya Pinder, MD, PhD
Timely initiation of therapy is a critical determinant of outcomes in cancer care. Time-to-treatment initiation (TTI) has been correlated with overall survival across multiple malignancies, yet disparities persist that may be influenced by social and geographic determinants.
“To investigate these factors in gynecologic cancers, we analyzed data from the National Cancer Institute’s Surveillance, Epidemiology and End Results Program (SEER), including 388,002 cases diagnosed between 2000 and 2022 with available TTI data,” said Rachel Hill, trainee associate member of the Cancer Center. “A delay in treatment initiation (DTI) was defined as TTI greater than 60 days from diagnosis, consistent with prior studies. Key variables included geographic region, metropolitan versus non-metropolitan county status, residence within a Purchased/Referred Care delivery area (PRCDA) and area-level median household income.”
On average, patients began treatment approximately 28 days after diagnosis. However, the risk of experiencing a treatment delay varied significantly by region with patients in the Midwest experiencing the lowest rates of delay.
The study also found that patients living in metropolitan counties were more likely to experience delays than those in non-metropolitan areas. Similarly, individuals residing within a Purchased/Referred Care delivery area (PRCDA) — a region where the Indian Health Service provides contract health services to members of federally recognized tribes — had increased odds of delayed treatment.
“Together, these findings highlight the complex ways geography, community resources and socioeconomic factors shape access to timely cancer care,” said Hill. “While treatment advances continue to improve outcomes, ensuring that patients can begin therapy without unnecessary delays remains critical. By identifying where disparities exist, researchers and health systems can work toward targeted strategies that improve access and equity in gynecologic cancer care, bringing timely, high-quality treatment within reach for all patients.”
Presentation at the 2026 Society for Teachers in Family Medicine Annual Conference
Anoosha SriTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Shanna Stryker, MD, MPH
Accurate data is critical for evaluating the effectiveness of cancer prevention programs, and this is particularly true for cervical cancer screening (CCS). Cervical cancer remains the fourth most common cancer among individuals assigned female at birth worldwide, with persistent human papillomavirus (HPV) infection accounting for approximately 95% of cases. When detected early, the five-year survival rate exceeds 90%, highlighting the importance of widespread, timely screening. In the U.S., the Health Resources and Services Administration monitors CCS rates at community health centers (CHCs) through the Uniform Data System (UDS), often linking funding to performance metrics.
At Equitas Health, a community health center focused on sexual and gender minority (SGM) health, recent UDS reporting indicated that cervical cancer screening (CCS) rates were below national averages. In 2022, the center implemented a CCS program incorporating self-collected primary HPV testing, which improved screening rates in certain SGM populations. However, data discrepancies emerged: some patients were flagged as overdue for screening despite being ineligible, i.e. those without a cervix.
“To address this, I conducted a three-month manual audit of all patients identified as overdue for cervical cancer screening (CCS),” said Anoosha Sri, trainee associate member of the Cancer Center. “This review quantified the frequency of misclassification and identified specific system-level factors contributing to errors. The findings provide actionable insights for improving data collection, integration and reporting, ensuring that CCS metrics more accurately reflect true care gaps.”
Between October 2025 and February 2026, weekly patient lists from the population health platform were reviewed. Each patient chart was manually assessed in the electronic medical record (EMR) to verify true eligibility for screening according to UDS and American Cancer Society guidelines. Discrepancies were tracked, coded by type and used to recalculate adjusted CCS rates.
“Preliminary findings from this audit reveal patterns in misclassification by the EMR and population health software, highlighting gaps between reported and actual screening needs,” Sri shared. “This work not only refines data accuracy but also informs targeted EMR interventions, enhancing both the quality of care and the validity of performance metrics — an essential step for linking quality improvement initiatives to funding and broader public health outcomes.”
Building on these insights, Sri emphasized that the recognition and support from this award will extend the impact of the audit beyond the clinic. By presenting these findings at a national conference, she will be able to engage directly with peers, experts, and policymakers, fostering discussions on improving equity and accuracy in screening metrics.
“Receiving this award is particularly meaningful as I embark on my research career,” she said. “It provides the opportunity to present my work at a national conference, engage with colleagues who share a commitment to equity and health promotion, and gain insights from diverse perspectives in disease prevention. Importantly, this platform allows our findings to reach decision-makers who influence screening practices and training nationwide, fostering broader dialogue about equitable measurement systems in cancer prevention and primary care.”
Journal: Leukemia
Courtnee Clough, PhDTrainee Associate Member, University of Cincinnati Cancer CenterMentor: Dan Starczynowski, PhD
Marked by hyperinflammation, bone marrow failure and high mortality, VEXAS syndrome is a clonal hematopoietic disorder that causes widespread inflammation, including recurrent fevers, skin rashes, relapsing chondritis and severe blood abnormalities like macrocytic anemia and thrombocytopenia. The molecular signature of VEXAS syndrome involves somatic mutations at methionine 41 (M41) in the E1 ubiquitin-activating enzyme UBA1, which trigger an isoform switch. However, the mechanisms driving disease pathogenesis remain poorly understood.
“To model VEXAS in vitro, we engineered a monocytic THP1 cell line to express the common UBA1 M41V mutation,” shared Courtnee Clough, PhD, trainee associate member of the Cancer Center.
These mutant cells reproduced key features of the disease, including abnormal UBA1 isoform expression, increased cytoplasmic vacuoles and activation of cellular stress pathways. Proteomic analysis showed disrupted ubiquitination and increased protein stress, particularly affecting inflammatory and stress-response signaling.
“We found that UBA1 M41V cells were especially sensitive to inhibition of E1 ubiquitin enzymes,” Clough explained. “Treatment with the E1 inhibitor TAK-243 reduced growth, impaired colony formation and increased cell death in mutant cells compared to wild-type cells. Notably, TAK-243 inhibited UBA6 more strongly than UBA1, suggesting that UBA6 may compensate for defective UBA1. Direct targeting of UBA6, either genetically or with the inhibitor phytic acid, selectively impaired growth of mutant cells while sparing normal cells.”
Together, these findings establish a human cell model of VEXAS and identify UBA6 as a potential therapeutic target for selectively eliminating UBA1-mutant cells. Furthermore, since UBA1 dysregulation has been implicated in many cancers, Clough and her team hope to expand this work in VEXAS syndrome to cancer more broadly.
As the project continues to evolve, this recognition marks an important milestone for the team and reinforces the broader significance of their findings. For Clough, the award not only acknowledges the scientific impact of the work but also highlights the collaborative effort behind bringing the study from concept to completion.
“Developing projects from the initial idea conception to a research publication is always one of the most rewarding parts of science,” she said. “This award is a testament to the commitment and collaboration of our team, and we are thankful that this collective work has been recognized. It also provides another valuable opportunity to share our findings with the broader community.”
Much of the project’s growth, Clough explains, has been made possible by the Cancer Center’s commitment to collaboration and scientific exchange. By investing in internal research programming and providing opportunities for broader dissemination, the Cancer Center ensures that promising discoveries benefit from rigorous interdisciplinary input.
“Access to opportunities to share my work — both within the Cancer Center community and on an international stage — has been pivotal in advancing this project,” she shared. “Presenting findings locally has allowed me to receive valuable feedback from colleagues across disciplines, refine my experimental approach and identify new collaborative directions. Engaging with the broader international research community has further strengthened the work by exposing it to diverse perspectives, emerging methodologies, and complementary expertise. Together, these experiences have not only sharpened the scientific rigor of the project but also expanded its potential impact beyond our institution.”
Journal: Science Advances
Over the past 15 years, immune checkpoint inhibitors (ICIs) have emerged as a transformative class of cancer therapeutics. By releasing inhibitory signals that restrain the immune system, these agents enable immune cells to recognize and eliminate tumor cells. ICIs have produced durable responses in many patients with advanced malignancies. However, a major limitation remains: some tumors exhibit an “immune-cold” phenotype, in which immune cells fail to effectively infiltrate the tumor microenvironment, resulting in resistance to ICI therapy. “In this study, we examined the role of the RAC1A159V mutation, the second most common RAC1 alteration, identified in several cancers including colorectal, lung, head and neck cancers and melanoma,” said Mingjun Cai, trainee associate member of the Cancer Center. “This mutation is associated with poorer patient outcomes, yet its contribution to therapeutic resistance has remained unclear.” Cai and her team have found that RAC1A159V functions as a potent driver of immune evasion, rendering tumors resistant to ICI therapy. Mechanistically, the mutation activates mTORC1 signaling, increasing metabolic activity in tumor cells while limiting the metabolic resources required for effective immune responses. RAC1A159V also suppresses chemokine production that normally recruits immune cells and reduces expression of genes involved in immune-mediated tumor killing. “Importantly, we found that rapamycin — an FDA-approved mTORC1 inhibitor — can reverse these effects,” Cai shared. “When combined with ICI therapy, rapamycin restored immune sensitivity in RAC1A159V tumors without damaging normal tissues. Together, these findings reveal a mechanism by which RAC1A159V promotes immune escape and suggests a clinically actionable strategy to overcome immunotherapy resistance. Pending validation in clinical studies, this approach could enable more personalized treatment strategies for patients whose tumors harbor this mutation.” For Cai, the award not only acknowledges the scientific rigor and translational potential of the study but also provides momentum for continuing to explore how tumor-intrinsic signaling pathways influence responses to immunotherapy. “This award recognizes the scientific rigor and translational relevance of my graduate research, and it really reinforces my commitment to mechanistic cancer immunology,” she said. “It further motivates me to investigate how tumor-intrinsic signaling pathways shape immune responsiveness and to develop strategies that improve the effectiveness of immunotherapies. The recognition also increases the visibility of this work, supports broader dissemination of our findings, and fosters continued mechanistic and translational investigation. In addition, it contributes to my professional development and opens new opportunities for collaboration and future funding.” Cai also credits the Cancer Center’s collaborative environment with helping shape the project. Access to investigators across disciplines and a culture that encourages open scientific exchange created opportunities to troubleshoot challenges and strengthen the rigor of the work. “My Cancer Center membership has given me access to a collaborative research community where I can easily seek advice, discuss experimental challenges and receive feedback from experts across different fields,” she said. “Many technical and conceptual questions in my project were clarified through discussions with other investigators and fellow trainees. This significantly improved the efficiency, rigor and quality of my research.”
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