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 Control research program and both the Cancer Biology & Immunology and Developmental Cancer Therapeutics research programs.

Overview | Eligibility | Evaluation | Timeline | Awardees

Bridge to Population Science

Applications are due on Monday, July 1, 2024, by midnight.

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 Control and Cancer Biology & Immunology. One award will support a partnership between Cancer 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.
  • At least one member of Cancer Control (full or affiliate) and at least one member of either Cancer Biology & Immunology or Developmental Cancer Therapeutics, who will serve in Co-PI roles.
  • Applicants must demonstrate a new collaboration.
  • 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

Timeline

Applicants are strongly encouraged to consult a biostatistician when developing the research design and methods of their proposals. If assistance is needed in identifying a biostatistician, please contact Dr. Betsy Hill (hille@musc.edu) as soon as possible, but no later than Monday, June 10, 2024.

Full applications are due on Monday, July 1, 2024, by midnight. After peer review, notifications of award will be made and the start date will be dependent on the status of human and animal studies protocol approvals. Applicants receiving a score just outside the funding range will be notified with the possibility of resubmitting their application for a subsequent RFA cycle.

2024 Awardees

head shot of a smiling doctor

Thomas Curran, M.D.

Cancer Control member

portrait of a scientist

Amy Engevik, Ph.D.

Cancer Biology & Immunology member

head shot of a smiling doctor

Mindy Engevik, Ph.D.

Cancer Biology & Immunology member

portrait of a scientist

Erin Forster, M.D.

Gastroenterologist

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.