Thomas J. Kelly
Professor
faculty
Pathology, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Thomas J. Kelly, Professor of Pathology at the University of Arkansas for Medical Sciences, investigates the mechanisms by which activated fibroblasts and tumor-associated macrophages interact to promote breast cancer growth and progression. His research focuses on whether activated fibroblasts can induce a shift in macrophages from an immune-activating M1 phenotype to an immune-suppressive M2 phenotype, and conversely, if immune-suppressive macrophages can trigger fibroblast activation. Previous work with Steven R. Post demonstrated that scavenger receptor A (SR-A)-mediated adhesion of macrophages to modified collagen leads to prostaglandin E2 (PGE2) production. This PGE2 has been shown to feedback on macrophages, modulating cytokine production towards an M2 phenotype, characterized by decreased TNF-alpha and increased IL-10 levels.
Currently, Kelly's laboratory is examining whether macrophage adhesion to fibroblast activation protein (FAP)-modified collagen also promotes the M2 phenotype. With a broad background in cellular biology, his research since 1992 has centered on two matrix-degrading enzymes: fibroblast activation protein-a (FAP) and heparanase. Kelly is an experienced Principal Investigator with a significant publication record, an h-index of 90, and over 29,500 citations, reflecting his extensive contributions to the field. He leads a research group and collaborates with several colleagues at the University of Arkansas for Medical Sciences, including Steven R. Post, Bolni Marius Nagalo, Martin J. Cannon, and Camila Simões.
Research Overview
We are defining the mechanisms of cross-talk between activated fibroblasts and tumor associated macrophages that results in facilitation of breast cancer growth and progression that ultimately kills people with breast cancer. Specifically, we are investigating if activated fibroblasts are capable of converting immune activating macrophages (M1) to immune suppressive macrophages (M2). We are also investigating if immune suppressive macrophages can cause fibroblast activation. Steven R. Post and I have shown that SR-A mediated adhesion of macrophages to modified collagen results in PGE2 production and this PGE2 feeds back onto the macrophages and modulates cytokine production towards an M2 phenotype as evidenced by decreased TNF-alpha and increased IL-10 production (Nikolic et al, 2015, J. Leukocyte Biol. Feb 25. pii: jlb.2A1014-471RR. [Epub ahead of print]). We are currently looking to determine if adhesion of macrophages to FAP-modified collagen also promotes the M2 phenotype. I am an experienced PI with a broad background in cellular biology, and since 1992, I have focused my research on two matrix degrading enzymes—fibroblast activation protein-a (FAP) and heparanase—and their relationship to breast cancer. For over 20 years, I have led an independent research group that studies mechanisms of breast cancer metastasis that has been continuously funded by DoD-BCRP, NIH, and Industry grants and contracts. As a result, I am experienced in successfully administering research projects (e.g., staffing, research protections and budget) and collaborating with both basic and clinical scientists. My research has been published in prestigious cancer journals, such as Cancer Research and Blood. Through this research, my team and I have developed extensive experience with FAP biology in breast cancer.
Metrics
- h-index: 90
- Publications: 459
- Citations: 29,580
Selected Publications
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Class A scavenger receptors promote tumor progression and induce a unique macrophage phenotype in a mouse model of spontaneous breast cancer (2026)
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Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade (2024)
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Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer (2024)
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<i>NR3C2</i> microdeletions—an underrecognized cause of pseudohypoaldosteronism type 1A: a case report and literature review (2024)
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The Tumor Microenvironment and Immune Response in Breast Cancer (2024)
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VT68.2: An Antibody to Chondroitin Sulfate Proteoglycan 4 (CSPG4) Displays Reactivity against a Tumor-Associated Carbohydrate Antigen (2023)
Grants & Funding
- Lymph liquid biopsy in cancer NIH Co-Investigator
- Fibroblast activation protein-alpha, a serine protease that facilitates metastasis by modification of diverse microenvironments US Department of the Army Principal Investigator
- Student Partners in Cancer Research and Education NIH/Nat. Cancer Institute Principal Investigator
- In vivo molecular laser detection and treatment of circulating cancer stem cells NIH Co-Investigator
- SR-A as a therapeutic target in breast cancer NIH Co-Investigator
- In vivo, noninvasive, ultrasensitive photoacoustic detection of early breast cancer metastasis in bone US Department of the Army Principal Investigator
- Suppressing Breast Cancer Tumor Growth with Inhibitor-a ActivX Biosciences, Inc Principal Investigator
- Partnership in Cancer Research (PCAR) NIH/Nat. Cancer Institute Principal Investigator
Collaboration Network
Top Collaborators
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
- Supplemental Table S1 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S3 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Table S2 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
- Supplemental Figure S4 from A Novel Bispecific Antibody Targeting EGFR and cMet Is Effective against EGFR Inhibitor–Resistant Lung Tumors
Showing 5 of 12 shared publications
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