Fecci worked at Duke University as an associate professor of Neurosurgery,Immunology,Pathology,[1] Biomedical Engineering,and Integrative Immunobiology.[2] At the same institution,he held the role of associate deputy director of the Preston Robert Tisch Brain Tumor Center[3] and holds principal investigator's designation.[4] He also co-directed the Duke Center for Brain and Spine Metastasis,[3] and holds the appointments of professor of Neurosurgery and Pathology there.[2] Additionally,in July 2025,he became chair of the Neurosurgery department at the University of Colorado School of Medicine.[5]
Research
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.[6] 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.[7] 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.[8]
Fecci highlighted that both CD4+ T cells[9] and Th cells are reduced in murine glioma models;however,Tregs account for a disproportionately large portion within the CD4 population.[10] He emphasized that dexamethasone reduces T cell proliferation and increases cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) on T cell surfaces.[11] In a group study,he identified that glioblastoma induced T cell dysfunction[12] and categorized it into exhaustion,senescence,anergy,tolerance,[13] and ignorance.[14]
Awards and honors
2013 –Synaptive Preuss Award,American Association of Neurological Surgeons (AANS) and the Congress of Neurological Surgeons (CNS)[15]
2016 –Prince Mahidol Youth Mentor Award,Prince Mahidol Award Foundation[16]
Selected articles
Fecci, P. E.; Mitchell, D. A.; Whitesides, J. F.; Xie, W.; Friedman, A. H.; Archer, G. E.; etal. (2006). "Increased regulatory T‑cell fraction amidst a diminished CD4 compartment explains cellular immune defects in patients with malignant glioma". Cancer Research. 66 (6): 3294–3302. doi:10.1158/0008-5472.CAN-05-3773. PMID16540683.
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