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David Munn, MD

Director of the Georgia Cancer Center Augusta University

  • Augusta GA

Dr. David Munn's research is focused on activating the body’s own immune system to fight cancer.

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Biography

Dr. David Munn's research is focused on activating the body’s own immune system to fight cancer. He and his research team work on discovering ways cancers suppress the immune system, and on identifying the molecular mechanisms that tumors use to escape from immune attack.

Dr. Munn teaches medical school classes in the histology of blood and lymphoid tissues. He participates in the professional education (conferences, teaching and supervision) of medical students, graduate students, post-doctoral fellows and junior faculty in his area of tumor immunology research.

Dr. Munn's research focuses on activating the immune system of children with cancer, so that they can mount an immune attack against the tumor. He has an active research laboratory in pre-clinical drug discovery, as well as implementing cutting-edge techniques for monitoring the immune response of children on immunotherapy clinical trials. He participates as a laboratory co-investigator on multiple clinical trials of new drugs and treatments that were invented in his laboratory.

Basic-science studies of the role of the indoleamine 2,3-dioxygenase (IDO) pathway in Tregs, including the regulation of the suppressor phenotype vs. destabilization and reprogramming during inflammation. Molecular mechanisms of inflammation-induced differentiation of immunogenic dendritic cells (DCs), and the suppression of these immunogenic DCs by IDO-activated Tregs. The translational goal of these studies is to develop orally bioavailable small-molecule drugs that induce differentiation of immunogenic DCs in tumors.

Basic and pre-clinical studies of immune response to dying tumor cells after chemotherapy; and synergy between conventional chemotherapy and novel forms of immunotherapy targeting Tregs and DCs.

Design and immune-monitoring of Phase I and Phase II clinical trials of IDO-inhibitor drugs in combination with chemotherapy, radiation, BTK-inhibitor drugs and checkpoint inhibitors. These include first-in-children pediatric trials, in conjunction with the Pediatric Immunotherapy Service and Dr. Theodore Johnson.

Areas of Expertise

Cancer Research
Tumor Immunology
IDO-Inhibitor Drugs
Lymphoid Tissues
Childhood Cancer
Cancers and the Immune System

Accomplishments

CureSearch Catapult Award

2023-2025

Education

Medical College of Georgia

M.D.

Medicine

1984

Mercer University

B.A.

Philosophy

1978

Media Appearances

David Munn, MD, appointed director of the Georgia Cancer Center

Augusta University News  online

2026-05-26

David Munn, MD, a physician‑scientist whose discoveries fundamentally reshaped the understanding of immune regulation in cancer, has been appointed director of the Georgia Cancer Center at the Medical College of Georgia. He has served as interim director since March, during which time he has worked to streamline clinical trials and recruit new basic and translational science researchers.

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AU scientists advance understanding of Nobel-winning immunology research

Augusta University News  online

2025-10-29

At Augusta University, David Munn, MD, co-director of the Pediatric Immunotherapy Program of the Medical College of Georgia at Augusta University, made seminal discoveries showing that Tregs are not always stable.

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Hyundai invests $400,000 in pediatric cancer research at Augusta University

Augusta University News  online

2025-08-27

“We really rely on people like Hyundai who understand the need and give hope to these kids,” said Munn, a professor of pediatric oncology for the Medical College of Georgia at Augusta University and co-director of the Pediatric Immunotherapy Program, which has developed several first-in-the-nation clinical trials for patients at Wellstar Children’s Hospital of Georgia.

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Articles

ANGI-04. HOST INTERFERON SIGNALING MODULATES EPITHELIAL-TO-MESENCHYMAL TRANSITION IN GLIOBLASTOMA INVASION THROUGH BRAIN CD73

Neuro-Oncology

2025

Glioblastoma (GBM) is an aggressive malignant brain tumor that invades adjacent normal brain tissue. The underlying mechanisms driving GBM invasion remain poorly understood. Unlike other solid tumors, GBM is infiltrated by various normal brain cells, including neurons, oligodendrocytes, oligodendrocyte progenitor cells (OPCs), microglia, and astrocytes. Recent studies suggest that brain cells infiltrating GBM may promote tumor growth and invasion. In this study, we observed that mouse GBM tumor GSC005 grown in immunodeficient (RAG1-KO, NSG) mice exhibited a more invasive phenotype compared to those in immunocompetent C57BL/6J mice. Immunofluorescence staining revealed the presence of vimentin+ and GFAP+ cells at the tumor-border interface, forming capsule-like structures around small tumor islands.

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IMMU-38. Single-cell RNA sequencing of cerebrospinal fluid in CARv3-TEAM-E treated glioblastoma

Neuro-Oncology

2025

Glioblastoma is a highly aggressive primary brain tumor in adults with limited treatment options. Although there has been continuing interest in employing the immune system to combat this disease, monoclonal antibody therapies, such as checkpoint modulating agents, have yet to demonstrate clinically transformative outcomes. Conversely, adoptive cell therapies including chimeric antigen receptor (CAR)-T cell therapies have shown early indications of efficacy in select GBM patients. In a recent report, a first-in-human trial of CARv3-TEAM-E T cells engineered to target the epidermal growth factor receptor variant III tumor-specific antigen (EGFRvIII) as well as wild-type EGFR through secretion of a T-cell-engaging antibody molecule (TEAM) demonstrated preliminary evidence of CAR activity.

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Lymph node macrophages drive immune tolerance and resistance to cancer therapy by induction of the immune-regulatory cytokine IL-33

Cancer Cell

2025

Apoptotic cells are immunosuppressive, creating a barrier in cancer treatment. Thus, we investigated immune responses to dying tumor cells after therapy in the tumor draining lymph node (TDLN). A key population responsible for clearing tumor material in the TDLN was medullary sinus macrophages (MSMs). Tumor debris phagocytosis by MSMs induces the cytokine IL-33, and blocking the IL-33 receptor (ST2) or deletion of Il33 in MSMs enhances therapy responses. Mechanistically, IL-33 activates T regulatory cells in TDLNs that migrate to the tumor to suppress CD8+ T cells. Therapeutically combining ST2 blockade, targeted kinase inhibitors, and anti-PD-1 immunotherapy increases CD8+ T cell activity promoting tumor regression.

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