Funding Awardees

Dr. Mark R. Green Young Investigator Awardees

Casey Langdon, Ph.D.

Assistant Professor, Pediatrics

Lu Han, Ph.D.

Assistant Professor, Biochemistry and Molecular Biology 

American Cancer Society Institutional Research Grant (ACS IRG) Awardees

Trisha Amboree, Ph.D.

Assistant Professor, Public Health Sciences

Mentors: Ashish A. Deshmukh, Ph.D., Kalyani Sonawane, Ph.D., Brian Orr, M.D., Britton Gibson, M.D., Elizabeth G. Hill, Ph.D., Jihad Obeid, M.D., Joni Nelson, Ph.D.

Project: An MUSC system-wide assessment of cervical cancer screening practices to enhance cervical cancer prevention in South Carolina

Cervical cancer is preventable, yet it remains a public health concern and a marker of disparity in South Carolina. Timely screening to detect and treat precancers is highly effective at preventing cervical cancer. To maximize the benefits of cervical cancer screening, it is important to reach high screening uptake, particularly using more sensitive screening strategies that test for human papillomavirus (HPV)—the virus that causes most cervical cancer.
Although primary HPV-based screening has been recommended for a while, many providers in the United States (US) have not adopted this strategy. MUSC Hollings Cancer Center is the only NCI-designated cancer center in South Carolina; therefore it is important to understand the health system’s approach to cervical cancer prevention (particularly evaluating the use of HPV-based screening tests and recommended screening strategies) and what barriers to screening exist for our patient population.

This project will conduct a MUSC system-wide assessment of current cervical cancer screening practices and identify potential barriers to screening experienced by our patient population. Additionally, as women with HIV (WHIV) have much higher risk of developing cervical precancer and cancer, and may experience unique challenges, this project will conduct a subpopulation assessment specifically focused on WHIV served by MUSC. The results of this study will be crucial to develop and implement targeted interventions to enhance cervical cancer prevention across MUSC, with the goal of reducing cervical cancers in the state.

Judit Jimenez-Sainz, Ph.D.

Assistant Professor, Biochemistry and Molecular Biology

Mentors: David Long, Ph.D., Kevin S. Hughes, M.D., Ozgur Sahin, Ph.D., Brian Neelon, Ph.D., Eduardo Caleiras, M.D.

Project: BRCA2 localization: Impact on cancer risk and treatment response

Each year in the U.S., approximately 20,000 breast and 3,000 ovarian cancer cases are linked to harmful BRCA2 mutations, often leading to poor long-term survival. While these mutations increase cancer risk, tumors with deleterious BRCA2 mutations typically respond well to platinum-based chemotherapy and PARP inhibitors.

However, genetic testing reveals that only about 25% of BRCA2 variants are classified as clearly harmful, while 40-50% fall into a gray area known as Variants of Uncertain Significance (VUS). These VUS, primarily missense variants, have unknown cancer risks and uncertain treatment responses.
BRCA2 is crucial for maintaining genomic stability by repairing damaged DNA through homology-directed repair (HDR) and protecting DNA replication forks. To function properly, BRCA2 must be located in the cell’s nucleus, where it helps repair DNA double-strand breaks.

Interestingly, research by Dr. Jimenez-Sainz has uncovered a paradox: when BRCA2 is mislocalized to the cytoplasm instead of the nucleus, cancer cells become more sensitive to targeted therapies like PARP inhibitors and platinum drugs—despite this mislocalization potentially contributing to cancer development.

Dr. Jimenez-Sainz’s project aims to define the cellular localization of BRCA2 and its partner protein RAD51 in gynecologic cancers and how specific BRCA2 missense mutations alter cellular pathways. By focusing on mutations in the DNA-binding domain and using proteomic analysis, this research seeks to establish BRCA2 localization as a potential diagnostic tool—paving the way for more precise cancer treatments and improved outcomes for patients with BRCA2 missense variants.

Souvik Seal, Ph.D. 

Assistant Professor, Public Health Sciences

Mentors: Peggi Angel, Ph.D., Brian Neelon, Ph.D., Anand Mehta, Ph.D., Kristin Wallace, Ph.D.

Project: Bayesian pipeline for comprehensive analysis of spatial proteomics datasets

The proposal aims to develop a unified, platform-independent software suite to analyze spatial proteomics datasets, such as MALDI mass spectrometry and multiplex immunofluorescence imaging, effectively addressing the underlying spatial autocorrelation and multicollinearity between molecules. Along with already established bioinformatics tools, the software will feature new statistical methods for spatially informed differential expression and multimodal spatial co-expression analysis using hierarchical Bayesian models.

Idea Awardees

Aaron Hobbs, Ph.D.

Assistant Professor, Biochemistry and Molecular Biology

Project: Exploiting the atypical KRAS G12R mutation to define novel therapeutic vulnerabilities in pancreatic cancer

Dr. Hobbs' award is funded in part by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related deaths in the U.S. and South Carolina. PDAC has a five-year survival rate of 12%. Approximately 95% of all PDAC cases harbor an activating KRAS mutation.

We previously demonstrated that KRAS mutations are not created equal. Two of these mutations are called G12D and G12R. Recently, we observed decreased collagen deposits in resected PDAC from patients with KRAS G12R. Collagen is deposited in the tumor microenvironment by cancer-associated fibroblasts. Critically, increased collagen in PDAC is associated with decreased overall survival. This suggests that KRAS mutant-selective therapeutic strategies targeting collagen production are feasible. It is not known how mutant KRAS promotes collagen production in the tumor.

We have engineered PDAC cell lines that are identical apart from the specific KRAS mutation. Using this model, we will determine how KRAS G12R signaling differs from KRAS G12D. We will define the mechanisms that dictate how specific KRAS mutations promote collagen production in PDAC. Once these mechanisms are determined, personalized therapies, based on KRAS mutation, can be developed to improve survival in all patients.

Daniel Sprague, M.D., Ph.D.

Assistant Professor, Biochemistry and Molecular Biology

Project: Exploiting ARID1A mutations to develop precision therapeutics in bladder cancer

Dr. Sprague's award is funded in part by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

Bladder cancer is one of the most common cancers in the United States, causing about 17,000 deaths annually. Sadly, survival rates have not improved much in the past 50 years. Many patients face treatments like surgery, chemotherapy, and immunotherapy that can be harsh and stop working over time. Only one drug is currently approved that targets specific genetic changes in bladder cancer, and it works in fewer than 20% of patients. This shows how urgently new options are needed.

One important genetic change in bladder cancer affects a gene called ARID1A. About 30% of patients have mutations in this gene, causing loss of ARID1A. Unfortunately, there are no medicines that directly fix this problem.

Our research is looking for new ways to treat patients with ARID1A-mutant bladder cancer. First, we will use advanced tools to scan the entire genome and find weak spots that cancer cells depend on when ARID1A is missing. Second, we will study tumor samples from patients who no longer respond to standard treatments, to see how their ARID1A mutations influence treatment choices.

This work aims to open the door to safer, more precise therapies.

Team Science Awardees

Abirami Sivapiragasam, M.D.
Associate Professor, Department of Medicine

Ozgur Sahin, Ph.D.
Professor, Department of Biochemistry & Molecular Biology

Shikhar Mehrotra, Ph.D.
Professor, Department of Surgery  

This team's award is funded in part by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

Improving the treatment landscape of TNBC by biomarker-guided novel therapies

Triple-negative breast cancer (TNBC) is one of the most aggressive and challenging forms of breast cancer, known for its early spread and limited treatment options. The standard treatment includes several chemotherapy drugs, such as anthracyclines, which can cause serious and lasting side effects, including heart damage. Some patients whose tumors have fewer immune cells or dense, scar-like (desmoplastic) tissue also respond poorly to immunotherapy, highlighting the need for more personalized and effective strategies.

Our team’s project aims to transform how TNBC is treated by developing more precise and less toxic therapies. We are studying immune cells within the tumor -called tumor-infiltrating lymphocytes (TILs)- to guide treatment decisions. Patients with high TIL levels often respond well to therapy and may achieve excellent results with shorter, less intensive chemotherapy. In contrast, patients with low TIL levels or tumors resistant to immunotherapy may benefit from new strategies designed to boost immune response, such as targeting resistance pathways or infusing immune cells directly into the body.

Through this research, we aim to improve outcomes, reduce side effects, and expand access to advanced, targeted treatments. This work will meaningfully impact patients with TNBC across South Carolina and serve as a model for improving care nationwide.

Bridge to Population Science Awardees

Trisha Amboree, Ph.D.

Cancer Prevention & Control member
Assistant Professor, Public Health Sciences

John Wrangle, M.D.

Developmental Cancer Therapeutics member
Associate Professor, Medicine

Are lung malignancies in our state associated with human papillomavirus infection?

Lung cancer disproportionately impacts South Carolina residents (10% higher 5-year rate of new diagnoses and 15% higher 5-year death rate compared to the national average). Screening is an effective strategy to prevent lung cancer with recommendations based mostly on smoking history, yet roughly 20% of lung cancers are among people who do not or have never smoked, thus identifying other risk factors is highly important.

Some studies have shown a potential association between human papillomavirus (HPV) and lung cancer; however, this relationship remains understudied in the US. Given the high burden of lung cancer in South Carolina, this project will conduct the first study of HPV prevalence in lung tumors using biospecimens from the Hollings Biorepository and Tissue Analysis (BTA) Shared Resource.

The Specific Aims are: (1) To determine the prevalence of HPV infection in lung cancer tissue by lung cancer type; and (2) To identify the HPV subtypes in lung cancer tissue by lung cancer type. The results from this study will provide much-needed pilot data on the relationship between HPV and lung tumors among MUSC patients and promote larger studies to fully investigate this relationship.

Antonis Kourtidis, Ph.D.

Cancer Biology & Immunology member
Associate Professor, Regenerative Medicine and Cell Biology

Kristin Wallace, Ph.D.

Cancer Prevention & Control member
Professor, Public Health Sciences

Type 2 diabetes promotes colorectal pro-tumorigenic transformation through disruption of an adherens junction-associated RNAi machinery

About 1 in 25 adults are anticipated to be diagnosed with colorectal cancer in their lifetime. Although systematic screening in the past decades has led to a steady decrease in colorectal cancer in older ages, there is an alarming increase in the incidence among the younger population (20-49 years old). In fact, early-onset colorectal cancer is expected to become the leading cause of death among ages 20-49 by 2030. Still, the root causes of the increase in early-onset colorectal cancer are poorly understood.

Type 2 diabetes (T2DM) is also increasing among the younger population and predisposes to colorectal cancer, providing a potential cause for the increased incidence in early-onset colorectal cancer. Although the biological mechanism linking T2DM to colorectal cancer is unknown, both cause damage to the cells of the colon lining which protects the body against diseases, including cancer. Our work has discovered that sustained damage to the colonic barrier can result in loss of function of microRNAs (miRNAs), i.e., small RNA molecules that suppress genes in healthy tissues but are disrupted in colorectal cancer and in diabetes.

Our goal is to investigate whether T2DM disrupts the colonic barrier and associated miRNAs to cause the upregulation of cancer-causing genes (i.e., oncogenes) that promote colorectal tumorigenesis. These studies have the potential to identify a biological mechanism to explain the relationship between colorectal cancer and T2DM which in turn could lead to the development of preventative and therapeutic interventions. Our hope is that this work will help decrease the burden of colorectal cancer, especially among the younger population.

Entrepreneurial Sciences in Cancer Awardees

Nancy Klauber DeMore, M.D.

Professor, Surgery 

Project: Reprogramming the tumor microenvironment in TNBC: Synergistic potential of IVT-8086 and TAM-modulating agents 

Dr. Klauber DeMore's award is funded in part by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

We have developed a new monoclonal antibody that targets a protein called secreted frizzled-related protein 2 (SFRP2), which plays a role in cancer progression. This antibody shows promise in treating triple-negative breast cancer (TNBC), a particularly aggressive form of breast cancer that currently has limited treatment options. In pre-clinical models, our antibody significantly reduced the growth of metastatic TNBC tumors.

One of the most exciting findings is how this antibody affects the immune system within the tumor environment. Tumors often contain immune cells called macrophages, which can either fight the cancer (M1 type) or support its growth (M2 type). Our antibody appears to shift the balance toward the M1 type, helping the body’s immune system attack the cancer more effectively.

This study will explore how the antibody causes this shift in macrophage behavior, which could lead to new strategies for enhancing immune responses in cancer treatment. Understanding this mechanism may also help improve therapies for other cancers where macrophages play a key role.

Overall, this research represents a promising step toward more effective treatments for TNBC and potentially other cancers, by combining targeted therapy with immune system modulation.

Pre-Clinical & Clinical Concepts Awardees

Joe Delaney, Ph.D.

Associate Professor, Biochemistry and Molecular Biology

Dr. Delaney’s award is funded by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

Pharmacologic Improvements in Treating Recurrent High-grade Serous Ovarian Cancer

Ovarian cancer in the U.S. will be diagnosed in over 19,000 women in 2025. Prognosis for metastatic disease is poor, with 5-year survival of approximately 30%. This study will investigate pharmacologic improvements to a commonly used chemotherapy to treat recurrent high-grade serous ovarian cancer.

Amanda Palmer, Ph.D.

Assistant Professor, Public Health Sciences

Dr. Palmer's award is funded in part by LOWVELO, MUSC Hollings Cancer Center's fundraising bike ride that channels 100% of rider-raised dollars into cancer research.

Biomarkers of Health Improvements After Abstinence from E-cigarettes and Combustible Cigarettes

Cigarette smoking has been decreasing among adults and, at the same time, use of e-cigarettes (vaping) has dramatically increased. Therefore, e-cigarettes are forecasted to surpass cigarettes as the most popular tobacco product used in the US.

E-cigarettes are battery-operated devices containing a liquid solution with nicotine, flavors, and other chemicals. While cigarette smoking is detrimental to health and a known risk factor for cancer, e-cigarettes are thought to be less harmful but not entirely risk-free, and less is known about e-cigarette use and cancer risk. Importantly, negative health effects from cigarette smoking can be reduced or even reversed following quitting smoking.

The purpose of the present study is to evaluate changes in biomarkers of health, specifically related to cancer, respiratory, and cardiovascular risk, that may occur when people stop using e-cigarettes. In the present study, participants who use e-cigarettes (and who never smoked, smoked in the past, or currently smoke) will be recruited to participate in a laboratory session followed by a week of nicotine abstinence. Throughout the study, participants will provide biological samples for analysis of DNA damage, immune functioning, inflammation, and respiratory functioning. Results will provide insight into the health benefits of quitting vaping, which will help to support future research grants evaluating the effectiveness and health outcomes of new treatments to help people quit vaping.

SCOR (Survivorship and Cancer Outcomes Research) Awardees 

Amanda Kastrinos, Ph.D.
Assistant Professor, Public Health Sciences

Kelly Hyland, Ph.D.
Assistant Professor, Psychiatry and Behavioral Sciences

Project: Characterizing dyadic communication challenges and support needs in young adults caring for a parent with metastatic cancer

Summary: Half of cancer caregivers in the U.S. are young adults (YA) (age 18-35) caring for a parent with cancer. YA child caregivers experience distressing emotional, social, and financial burdens given their place in the lifespan, including a significant shift in family roles. Caregiving for a parent with metastatic cancer (e.g., metavivor) is further complicated by significant uncertainty and variability in prognosis, goals of care, and caregiving needs over time.

Open communication within the survivor-caregiver dyad is associated with better physical and psychological outcomes for both parties. However, YA child caregivers and metavivor parents face unique communication challenges, such as parents withholding medical information to shield children from distress and children withdrawing from their parent as a strategy to cope. These communication patterns can increase anxiety, uncertainty, and distress in the dyad.

This study will characterize communication challenges and support needs in the YA child caregiver-parent metavivor dyad to inform the development of a dyadic behavioral intervention specifically tailored to this unit and their needs. Metavivors and caregivers will participate in in-depth interviews and complete an online questionnaire. Findings will provide critical pilot data to inform the development of a tailored dyadic intervention to improve dyadic communication and quality of life.