Peter Edward Fecci | |
|---|---|
| Occupations | Neurosurgeon and academic |
| Academic background | |
| Education | Bachelor of Science Doctor of Medicine Doctor of Philosophy |
| Alma mater | Cornell University Duke University |
| Academic work | |
| Institutions | Duke University University of Colorado School of Medicine |
Peter Edward Fecci is a neurosurgeon and academic. He is a professor of neurosurgery and pathology at Duke University School of Medicine.
Fecci's research has focused on brain tumor immunology and immunotherapy, and T cell dysfunction in glioblastoma and other intracranial cancers. He has received the Synaptive Preuss Award from the American Association of Neurological Surgeons (AANS) and the Congress of Neurological Surgeons (CNS).
Fecci received his Bachelor of Science degree from Cornell University, followed by a Doctor of Medicine and Doctor of Philosophy from Duke University. He also completed a Neurosurgical residency at Massachusetts General Hospital.
Fecci worked at Duke University as an associate professor of Neurosurgery, Immunology, Pathology, Biomedical Engineering, and Integrative Immunobiology. At the same institution, he held the role of associate deputy director of the Preston Robert Tisch Brain Tumor Center and holds principal investigator's designation. He also co-directed the Duke Center for Brain and Spine Metastasis, and holds the appointments of professor of Neurosurgery and Pathology there. Additionally, in July 2025, he became chair of the Neurosurgery department at the University of Colorado School of Medicine.
In a collaborative research, Fecci conducted an immunocompetent study with an emphasis on lung adenocarcinoma and observed that TIM-3 expression significantly contributed to tumor relapse after anti-PD-1 treatment. He also demonstrated that the activated epidermal growth factor receptor (EGFR) pathway promoted immune escape by increasing the levels of PD-1 and PD-L1. Additionally, he examined the presence of STK11/LKB1 in KRas-mutated tumors, determining that it lowers PD-L1 levels, reduces T-cell infiltration, and increases T-cell exhaustion markers.
Fecci highlighted that both CD4+ T cells and Th cells are reduced in murine glioma models; however, Tregs account for a disproportionately large portion within the CD4 population. He emphasized that dexamethasone reduces T cell proliferation and increases cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) on T cell surfaces. In a group study, he identified that glioblastoma induced T cell dysfunction and categorized it into exhaustion, senescence, anergy, tolerance, and ignorance.