Thomas J. Kelly
Professor
Also affiliated: Rutgers, The State University of New Jersey (2021); University of California, Riverside (1998); University of Notre Dame (1967–1982); University of North Carolina at Chapel Hill (1982–2021); University of Southern California (2014–2015); New Jersey Institute of Technology (2023–2025); Australian Sports Commission (2010); The Honourable Society of Lincoln's Inn (1993); San Francisco General Hospital (1995–1996); National Institutes of Health (1971–1989); Arkansas Children's Hospital (2024); Salk Institute for Biological Studies (1993); Agricultural Research Service (1982–1998); Agricultural Marketing Service (1982); Battelle (2011–2015); Johnson & Johnson (United States) (2025); Memorial Sloan Kettering Cancer Center (2003–2021); United States Department of Agriculture (1982–1996); Howard Hughes Medical Institute (1986); University of Bonn (1991); Harvard University (1969); University of Kentucky (2001); Johns Hopkins University (1970–2004); University of Liverpool (1952–1971); Thomas Jefferson University (2023–2025); Emory University (1987); University of Illinois Urbana-Champaign (1976); University of St Andrews (1991); Iowa State University (1979); University of California, San Francisco (1988–1997); Baylor College of Medicine (2001); Georgetown University (1989–2008); United States Naval Academy (2024); Universität Innsbruck (1998); United States Military Academy (1986); Princeton University (2008); Trinity College Dublin (2023); University of Arkansas Medical Center (1997–2015); Johns Hopkins Medicine (1970–2002); Georgetown University Medical Center (1994–2008); St James's University Hospital (2025); Cancer Institute (WIA) (2025); Wexford General Hospital (2023); Weiss Memorial Hospital (2008); Center for Environmental Health (1996); Johns Hopkins University Applied Physics Laboratory (1973); University of Manchester (2023); University of Florida (2025–2026); University of Illinois Chicago (2019–2021); Kettering University (2004–2021); University of Oxford (1993); University of Chicago (2007–2021); University of Chicago Medical Center (2021); Beltsville Human Nutrition Research Center (1990); Clayton Foundation (1980); Central Arkansas Veterans Healthcare System (2002); Springhouse (2016–2024); Cell Biotech (South Korea) (1986); Université de Fianarantsoa (2022); Dana-Farber Cancer Institute (1990); Med Center (2022); Merck Biopharma Co., Ltd. (Japan) (1990); Mayo Clinic in Arizona (2011); Beltsville Agricultural Research Center (1981–2000); Highland Community College - Illinois (2022); Cancer Research Center (1994–2011); Winthrop Rockefeller Foundation (2010–2025); Frederick National Laboratory for Cancer Research (1991); Institute of Behavioral Sciences (2003); National Institute of Allergy and Infectious Diseases (1971–1973); Stanford Medicine (1973); National Cancer Institute (1991); Janssen (United States) (2024); St. James's Hospital (2023); Arkansas Department of Agriculture (2016); Jefferson Hospital for Neuroscience (2023); Ysbyty Gwynedd Hospital NHS Trust (2015); Neurology, Inc (2022); Indiana University School of Medicine (2021); Rutgers New Jersey Medical School (2021); Weizmann Institute of Science (1987); Case Western Reserve University (2008); Stony Brook University (2022); University of Maryland, College Park (1986); University of Pennsylvania (1977–1979); TechnipFMC (United States) (2009); The University of Texas at Austin (1980–2010); Michigan State University (1982); Kelly Services (United States) (1999–2000); Stanford University (1973)
Faculty Researcher
Pathology, College of Medicine
Upstream record may be merged OpenAlex, the source of these figures, lists 91 institutions in 12 countries for this author record — a pattern that usually means it combines several researchers with similar names. The totals above may include work by other people.
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Thomas J. Kelly is a Professor in the Department of Pathology at the University of Arkansas for Medical Sciences. His research focuses on defining the mechanisms of cross-talk between activated fibroblasts and tumor-associated macrophages that contribute to breast cancer growth and progression. Specifically, his work investigates whether activated fibroblasts can convert immune-activating macrophages (M1) to immune-suppressive macrophages (M2), and conversely, if immune-suppressive macrophages can induce fibroblast activation.
Kelly and Steven R. Post have demonstrated that macrophage adhesion to modified collagen, mediated by scavenger receptor A (SR-A), results in prostaglandin E2 (PGE2) production. This PGE2 then feeds back onto the macrophages, modulating cytokine production towards an M2 phenotype, characterized by decreased TNF-alpha and increased IL-10. Current investigations are examining if macrophage adhesion to fibroblast activation protein-alpha (FAP)-modified collagen also promotes this M2 phenotype. Kelly possesses a broad background in cellular biology, with research since 1992 concentrating on two matrix-degrading enzymes: fibroblast activation protein-alpha (FAP) and heparanase.
With an h-index of 90, over 455 publications, and more than 29,000 citations, Kelly is recognized as a highly cited researcher. His laboratory leads research groups and maintains an active website. Key collaborators at the University of Arkansas for Medical Sciences include 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: 456
- Citations: 29,783
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
As listed on this researcher's institutional profile.
- 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
- Anti-tumor effects of inhibitors of fibroblast activation protein-alpha and other dipeptidyl peptidase and structural homologs (DASH) proteases Ferring Research Limited Principal Investigator
- Role of heparanase in osteolytic bone metastasis NIH/Nat. Cancer Institute via University of Alabama at Birmingham Principal Investigator
- Fibroblast-macrophage interactions induce a tumor-promoting microenvironment NIH/National Institutes of Health Co-Principal Investigator
- Photoswitchable nanoprobes for in vivo flow cytometry NIH Co-Investigator
Collaboration Network
Top Collaborators
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- VT68.2: An Antibody to Chondroitin Sulfate Proteoglycan 4 (CSPG4) Displays Reactivity against a Tumor-Associated Carbohydrate Antigen
- The Tumor Microenvironment and Immune Response in Breast Cancer
Showing 5 of 6 shared publications
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Class A scavenger receptors promote tumor progression and induce a unique macrophage phenotype in a mouse model of spontaneous breast cancer
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Class A scavenger receptors promote tumor progression and induce a unique macrophage phenotype in a mouse model of spontaneous breast cancer
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
- Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy
- Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer
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