Drew Pardoll
Johns Hopkins University, MD·Microbiology & Immunology
Tumors can protect themselves by switching off the immune cells that would otherwise attack them. One major off-switch is PD-1, a receptor on activated immune cells.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Pharmacology
- Topics
cancer immunotherapy
immune checkpoint blockade
immunotherapy resistance
- Grants
- 2 known grants, through May 2027
What they work on
- Identify molecules made by regulatory T cells (Tregs), immune cells that suppress other immune cells, that are found specifically in tumors of patients who do not respond to anti-PD-1 or anti-PD-L1 therapy.
- Define pathways inside tumor cells that cause resistance to PD-1 pathway blockade, building on gene expression profiling that linked tumor-intrinsic programs to treatment failure.
- Characterize immune and stromal factors in the tumor microenvironment that shape response or resistance to anti-PD-(L)1 drugs, using the AstroPath multi-layer tissue imaging platform.
- Define molecules and pathways that regulate anti-cancer immune responses, and combine animal models with analysis of patient samples to find targets and drug combinations that overcome immunotherapy resistance.
- Develop and test new immunotherapies and predictive biomarkers in clinical trials, translating cancer immunology discoveries into standard cancer care.
More about the research
It shuts those cells down when it binds PD-L1 or PD-L2, proteins that tumors can display. Drugs that block this interaction, called anti-PD-1 or anti-PD-L1 antibodies, are now approved for many cancers. Tests for PD-L1 in tumor biopsies help choose which patients receive them. Yet about 80% of treated patients do not benefit. This work studies why patients resist these drugs and how to overcome that resistance, from basic studies in mice to clinical trials.
Why it matters
Immune checkpoint drugs that block PD-1 or PD-L1 help some patients with advanced cancer, but about 80% of treated patients do not respond or later relapse. Finding the immune, tumor and tissue factors behind this resistance could lead to biomarkers that predict who will benefit. It could also lead to drug combinations that make immunotherapy work for more patients with melanoma, lung, pancreatic, colorectal and other cancers.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jun Wang
New York University, NY·Microbiology & Immunology
Determine whether Siglec-15, a tumor-associated immune brake, also suppresses myeloid cells such as macrophages, and identify the receptors it binds on myeloid cells and T cells.
Guangyong Peng
Washington University in St Louis, MO·Microbiology & Immunology
Identify how human Treg cells rewrite lipid metabolism and fate in responder T cells, focusing on the energy sensor AMPK, ATM DNA-damage signaling, and MAPK signaling.
Mekhail Anwar
University of California-San Francisco, CA·Biomedical Engineering
Develop and test PET imaging of granzyme B, a molecule released by active killer T cells, and of tumor neutrophil levels to detect early response or resistance to PD-1/PD-L1 checkpoint inhibitors in mouse tumor models.
The school
Johns Hopkins University: 100 labs on PI Pages, $4.1B a year on research, 622 research doctorates a year.
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