Thomas J. Kelly

High Impact

Professor

UAMS

Also affiliated: 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); Merck & Co., Inc., Rahway, NJ, USA (United States) (1990); San Francisco General Hospital (1995); National Institutes of Health (1971–1989); Arkansas Children's Hospital (2024); Salk Institute for Biological Studies (1993); Agricultural Research Service (1982–2000); San Francisco VA Medical Center (1995); Battelle (2015); Mayo Clinic (2011); Memorial Sloan Kettering Cancer Center (2003–2021); United States Department of Agriculture (1981–2000); 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 (1988–1995); Baylor College of Medicine (2001); Georgetown University (1989–2008); Universität Innsbruck (1998); Princeton University (2008); Trinity College Dublin (2023); University of Arkansas Medical Center (2003–2022); Johns Hopkins Medicine (1973–2002); Georgetown University Medical Center (2008); St James's University Hospital (2025); University of Florida (2026); University of Oxford (1993); University of Chicago (2007–2021); University of Chicago Medical Center (2021); Central Arkansas Veterans Healthcare System (2002); USC Norris Comprehensive Cancer Center (2015); Dana-Farber Cancer Institute (1990); Beltsville Agricultural Research Center (1981–2000); Frederick National Laboratory for Cancer Research (1991); National Institute of Allergy and Infectious Diseases (1971–1973); Stanford Medicine (1973); National Cancer Institute (1991); St. James's Hospital (2023); Ysbyty Gwynedd Hospital NHS Trust (2015); Neurology, Inc (2022); Georgetown Lombardi Comprehensive Cancer Center (1994–2008); Rutgers New Jersey Medical School (2021); Weizmann Institute of Science (1987); University of Maryland, College Park (1986); University of Pennsylvania (1977–1979); The University of Texas at Austin (1980); Michigan State University (1982)

Pathology, College of Medicine

89 h-index 433 pubs 29,180 cited

Upstream record may be merged OpenAlex, the source of these figures, lists 59 institutions in 6 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

Links

ORCID Lab Website Research Group UAMS TRI Profile

OverviewAI-generated summary

Thomas J. Kelly's research focuses on understanding the mechanisms by which activated fibroblasts and tumor-associated macrophages interact to promote breast cancer growth and progression. His work investigates whether activated fibroblasts can transform immune-activating macrophages (M1) into 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), leads to prostaglandin E2 (PGE2) production. This PGE2, in turn, feeds back on the macrophages, shifting their cytokine production towards an M2 phenotype, characterized by decreased TNF-alpha and increased IL-10. Current investigations are exploring if macrophage adhesion to fibroblast activation protein (FAP)-modified collagen also promotes this M2 phenotype. Kelly possesses extensive experience as a Principal Investigator with a broad background in cell biology. Since 1992, his research has centered on two matrix-degrading enzymes: fibroblast activation protein-alpha (FAP) and heparanase.

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: 89
Publications: 433
Citations: 29,180

Positions

Professor 1992–present

University of Arkansas for Medical Sciences Pathology, College of Medicine Institutional directory

Selected Publications

Class A scavenger receptors promote tumor progression and induce a unique macrophage phenotype in a mouse model of spontaneous breast cancer (2026)

DOI OpenAlex
Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade (2024)

4 citations DOI OpenAlex
Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer (2024)

4 citations DOI OpenAlex
<i>NR3C2</i> microdeletions—an underrecognized cause of pseudohypoaldosteronism type 1A: a case report and literature review (2024)

1 citation DOI OpenAlex
The Tumor Microenvironment and Immune Response in Breast Cancer (2024)

2 citations DOI OpenAlex
VT68.2: An Antibody to Chondroitin Sulfate Proteoglycan 4 (CSPG4) Displays Reactivity against a Tumor-Associated Carbohydrate Antigen (2023)

3 citations DOI OpenAlex

View all publications on OpenAlex →

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