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

Lu Han, Ph.D.

Assistant Professor, Biochemistry & Molecular Biology

Mentor: Ozgur Sahin, Ph.D.

Project: GATA6 Functions in Pancreatic Cancer Associated Fibroblasts to Regulate Tumor Progression and Immune Suppression

Dr. Han'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.

Pancreatic cancer is one of the deadliest types of cancer. The normal pancreas is mainly made up of cells called epithelial cells and some sparse cells called fibroblasts. When there are mistakes in the DNA of epithelial cells, these normal epithelial cells can change into tumor cells, which leads to pancreatic cancer. When this happens, the fibroblasts also grow drastically and make up more than half of the tumor tissue. Fibroblasts can stop the tumor from growing, but sometimes they can also help the tumor grow. How exactly this works is still not clear.

This proposal will test the idea that some types of fibroblasts keep some features from the fetal developmental stage, and these features might limit tumor growth in pancreatic cancer. To do this, the Han laboratory will study samples from patients who have pancreatic cancer and will use special mouse models that mimic how cancer develops. The results of this study will show that these fetal-like features might be an important way the body uses to fight cancer. Ultimately, learning more about fibroblasts could help find new ways to slow tumor growth and prolong patient survival.

Kelly Hyland, Ph.D.

Assistant Professor, Psychiatry & Behavioral Sciences

Mentor: Katherine Sterba, Ph.D.

Project: LiveWell mBC: Pilot Test of an Adapted Dialectical Behavioral Therapy Skills Training Program in Groups of Women Living With Metastatic Breast Cancer

Dr. Hyland'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.

People with metastatic breast cancer are living longer because of better treatments, but longer survival often comes with ongoing emotional distress, physical symptoms, and uncertainty about the future. Many patients experience depression, anxiety, and reduced quality of life, and current support programs are not always designed to meet their changing emotional needs. This study will test a new skills training program called LiveWell mBC, designed specifically to help women live well with metastatic breast cancer.

LiveWell mBC teaches skills adapted from Dialectical Behavioral Therapy, an evidence-based psychotherapy. Women learn practical tools to manage emotions, cope with stress, live in the present moment (mindfulness), and communicate effectively. The program includes an orientation and eight weekly small-group sessions delivered by telehealth. Early results from a small pilot study showed high satisfaction and attendance, along with meaningful improvements in emotional well-being and quality of life.

This new study will enroll 48 women receiving care at Hollings Cancer Center and randomly assign them to either LiveWell mBC or usual care. Researchers will evaluate participation, satisfaction, and changes in distress, well-being, symptoms, and quality of life. Participant interviews will also help refine the program. Results will guide a larger future trial and may improve supportive care for people living with metastatic cancer. 

Michelle Mollica, Ph.D., MPH, RN, OCN, FAAN

Associate Professor, Nursing

Mentor: Jennifer Dahne, Ph.D.

Project: PRIMary care Engagement in Survivorship (PRIMES): A Mixed Methods Study

Dr. Mollica'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.

This study focuses on improving care for colorectal cancer survivors. After a cancer diagnosis, survivors often face ongoing physical and emotional challenges, yet follow up care is frequently fragmented between oncology teams and primary care providers. Survivors may be unsure who to contact for their health care concerns, while clinicians lack clear roles and effective ways to communicate, leading to unmet needs, duplicated services, and poor health outcomes.

To address these challenges, we aim to develop a practical, technology-supported blueprint for shared survivorship care: PRIMary care Engagement in Survivorship (PRIMES). This study will seek perspectives of colorectal cancer survivors, oncology clinicians, and primary care providers to better understand current gaps and identify solutions that fit real world clinical settings. Through surveys, interviews, and focus group discussions, the research team will clarify care responsibilities and design the PRIMES intervention blueprint to improve communication and coordination across primary care and oncology.

The long term goal of PRIMES is to support a sustainable, team-based model of survivorship care that improves patient experiences, care quality, and health outcomes. By strengthening connections between oncology and primary care, PRIMES aims to ensure survivors receive coordinated and comprehensive follow-up care to address their needs.

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, Medicine

Ozgur Sahin, Ph.D.

Professor, Biochemistry & Molecular Biology

Shikhar Mehrotra, Ph.D.

Professor, Surgery

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

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.

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

Project: 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

Project: 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 

Antonis Kourtidis, Ph.D.

Associate Professor, Regenerative Medicine and Cell Biology

Project: Engineering junctional RNAi therapeutics as tumor suppressors

About 80-90% of all cancers arise from the epithelium, the tissue that covers our organs and bodies. Cells in epithelial tissues are tightly connected with each other through protein complexes called cell-cell junctions that also form the epithelial barrier that protects our organs from environmental insults. Disruption of cell-cell junctions and of the barrier is a universal feature of tumors.

Although this disruption has traditionally thought to be the result of oncogenic transformation, our work in recent years has revealed that it is actually causative: disruption of cell-cell junctions promotes pro-tumorigenic transformation. We have particularly found that the junctions exert this function through a protein called PLEKHA7 that in normal cells engages the RNA interference (RNAi) machinery and microRNAs (miRNAs) to suppress oncogene expression. However, we have also found almost universal disruption of this cell junction-RNAi mechanism in cancers, such as in colorectal cancer (CRC), whereas restoration of this mechanism in colon cancer cells suppresses their growth in mice.

In this project, the Kourtidis lab teams up with the Jakymiw lab, an expert in peptide- and RNA-based therapeutics, to develop and optimize novel tools that can be used to restore the junctional-RNAi machinery in tumors and suppress their growth. Since disruption of this mechanism seems to be universal in epithelial tumors, which account for more than 2/3rds of all tumors, the goal is to develop a novel therapeutic with potentially broad applicability, which restores this otherwise naturally occurring tumor-suppressing mechanism, therefore with potentially minimal side effects.

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

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.