Stephanie K. Dougan, PhD
Investigator, Hale Family Center for Pancreatic Cancer Research
Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute
Associate Professor of Immunology, Harvard Medical School
Assistant Professor of Microbiology, Harvard Medical School
Bio
Dr. Stephanie Dougan received her PhD in immunology from Harvard University, where she studied lipid antigen presentation by CD1d and NKT cell development with Richard Blumberg. She then performed a postdoctoral fellowship with Hidde Ploegh at the Whitehead Institute, where she became adept in somatic cell nuclear transfer and embryo manipulation for the purpose of generating transnuclear and CRISPR genome-modified mice.
Dr. Dougan joined the faculty at Harvard Medical School (HMS) and Dana-Farber Cancer Institute in 2014, where her lab uses unique mouse models to study the immune response to tumors. She is particularly interested in tumors that do not induce a CD8 T cell response at baseline, and has been using pancreatic cancer as a model to develop new immunotherapies for non-T cell infiltrated tumors.
Dr. Dougan is the course director for the Harvard Immunology Summer Undergraduate Program, the co-director for the graduate school class Immunology 201, and the course director for an Advanced Integrated Science course in immunology for third-year HMS medical students.
Research Interests
Our specific interest is in understanding why pancreatic cancers are so refractory to immunotherapy. We do not fully understand how tumor-specific T cells infiltrate densely fibrotic pancreatic tumors, or how to recruit more activated T cells to the tumor mass. Our lab is developing novel strategies to address this question.
We take a comprehensive approach, combining in vitro immunology assays and novel transnuclear and CRISPR genome-edited mice to probe the determinants of anti-tumor immunity. We are collaborating with other members of the Hale Family Center for Pancreatic Cancer Research to profile the pancreatic tumor microenvironment, and to test how targeted therapies affect the immune response to pancreatic cancer.