Steven N. Fiering, PhD
Professor of Microbiology and Immunology
Professor of Genetics
Professor of Genetics
Microbiology and Immunology
Stanford, Ph.D., 1990
University of Michigan, BS, 1975
Dr. Fiering received his Bachelor of Science from the University of Michigan in 1975, and his Doctorate from Stanford in 1990. After postdoctoral work as an NIH research fellow and research associate at the Fred Hutchinson Cancer Research Center, Dr. Fiering joined the faculty of the Department of Microbiology at Dartmouth Medical School in 1997.
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
Dartmouth Medical School
Rubin Bldg. HB 7936
1 Medical Center Drive
Lebanon NH 03756
My lab is primarily focused on developing novel immune-based strategies for treating cancer. The basic idea is to inject various immunostimulatory reagents, including live attenuated microorganisms into a primary tumor. This treatment can stimulate an immune response against the tumor and develop systemic anti-tumor immunity that protects against metastatic disease.
We are also interested in mouse models of cancer and are developing novel mouse models. The influence of tobacco smoke exposure on the innate immune system is another area of research in the lab.
Human Genetics graduate course
Meditative Movement as a Treatment for Pulmonary Dysfunction in Flight Attendants Exposed to Second-Hand Cigarette Smoke: Study Protocol for a Randomized Trial.
IL-15 AGONISTS OVERCOME THE IMMUNOSUPPRESSIVE EFFECTS OF MEK INHIBITORS.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.
Myeloid Acyl-CoA:Cholesterol Acyltransferase 1 Deficiency Reduces Lesion Macrophage Content and Suppresses Atherosclerosis Progression.
In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells.
Virus-based nanoparticles as platform technologies for modern vaccines.
Toward Localized <i>In Vivo</i> Biomarker Concentration Measurements.
Registered report: Biomechanical remodeling of the microenvironment by stromal caveolin-1 favors tumor invasion and metastasis.
Structure-based redesign of lysostaphin yields potent antistaphylococcal enzymes that evade immune cell surveillance.
Depletion of T cell epitopes in lysostaphin mitigates anti-drug antibody response and enhances antibacterial efficacy in vivo.