Bridge to Population Science Award

The purpose of the Bridge to Population Science Award is to provide pilot funding that will foster new and successful partnerships between members of the Cancer Prevention & Control research program and both the Cancer Biology & Immunology and Developmental Cancer Therapeutics research programs.

Overview | Eligibility | Evaluation | Awardees

Overview

MUSC Hollings Cancer Center leadership anticipates distributing two awards of $50,000 per year for one year with the possibility of no cost extensions for up to one year. Extensions will require prior approval. One award will support a partnership between Cancer Prevention & Control and Cancer Biology & Immunology. One award will support a partnership between Cancer Prevention & Control and Developmental Cancer Therapeutics.

Sources of funding for the award include the Hollings Cancer Center Support Grant (P30 CA138313), fundraising from the LOWVELO bike ride, or other Hollings philanthropy/foundation accounts. PIs are expected to obtain regulatory approvals (e.g., IACUC and IRB) within three months of award decision. Please note that the funding cannot be released until required approvals have been obtained for any human and animal subject protocols and copies have been provided. For more information or questions regarding the Hollings Bridge to Population Science Award, eligibility, or the application process, please contact Renee Steffen (steffenr@musc.edu).

Eligibility

• Proposed research must be cancer relevant.
• Must be a Hollings member (full or affiliate).
• At least one member of Cancer Prevention & Control and at least one member of either Cancer Biology & Immunology or Developmental Cancer Therapeutics, who will serve in Co-PI roles.
• Applicants that demonstrate a new collaboration will be prioritized.
• Applicants must make use of at least one of the seven Hollings shared resources.
• Applicants are encouraged but not required to include partnerships with South Carolina State University.
• All awarded PIs are encouraged to participate as a registered rider in the annual LOWVELO bike ride.

Evaluation

• Priority will be given to early stage investigators.
• Review criteria include:
  
  • Standard NIH criteria
  • Potential to lead to future NIH funding

2025 Awardees

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.

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

About 1:25 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.

2024 Awardees

Sphingolipid Metabolism in Regulation of Tumor Immunity to Predict BCG Treatment Response

This 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.

For patients with non-muscle invasive bladder cancer (NMIBC), one of the most common types of bladder cancer, there is an unmet clinical need in predicting which patients will respond to front-line bacillus Calmette-Guerin (BCG) treatment. To address this need, our team will investigate a novel pathway through which sphingolipid metabolism and signaling shape the immune microenvironment in the bladder to be unresponsive to BCG therapy. We will utilize clinical data and tumor samples from patients with bladder cancer treated at MUSC Hollings Cancer Center to measure sphingolipid biomarker in the collected tumor samples. With findings from this study, we will be able to determine the impact of sphingolipid metabolism and signaling on BCG-treatment response.

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Elucidating the role of Myosin 5b in the progression on IBD associated colorectal cancer

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.

Inflammatory bowel disease (IBD) is a common condition where the digestive tract gets inflamed. People with IBD have a higher chance of dysplasia, which can lead to polyps, which can become cancerous over time. This transformation from dysplasia to cancer is a gradual process, and it's essential to detect and remove these precancerous growths through regular screenings, like colonoscopies.

Some IBD patients have low grade dysplasia that can't be seen during the colonoscopy, and these patients need special testing with random samples. However, not everyone sticks to this routine because it can be expensive, inconvenient and has some risks. Our team recently identified an important protein that regulates intestinal epithelial dysplasia: Myosin 5b.

Myosin 5b is a molecular motor which traffics proteins to the upper membrane of intestinal cells. We identified that Myosin 5b is the key transporter for the PAR complexes; proteins which control cell polarity. We found that mice lacking Myosin 5b had mislocalized PAR complex proteins, defects in cell polarity and increased proliferation: all hallmarks of dysplasia. We also found that inflammation was able to reduce Myosin 5b in a mouse model of colitis. Consistent with our animal models, we found that Myosin 5b was decreased in biopsies from IBD patients and almost completely absent from colorectal cancer samples.

Based on these preliminary data, we hypothesize that IBD patients with low grade dysplasia that do not progress to high grade dysplasia will have more Myosin 5b than patients that progress to colorectal cancer. Our long-term goal is to better understand and identify mechanisms behind cancer progression and identify new targets for cancer prevention. In Aim 1, we will examine the distribution of PAR complex proteins in patient tissue specimens. In Aim 2, we will inhibit Myosin 5b in human intestinal organoids and monitor dysplasia progression. Our research aims to show whether Myosin 5b can be a helpful marker in predicting which IBD patients will go onto develop cancer.