Thomas J. Kelly

High Impact

Professor

University of Arkansas for Medical Sciences

faculty

Pathology, College of Medicine

90 h-index 458 pubs 29,477 cited

Research Areas

Genomics and Chromatin Dynamics Immune Cell Function and Interaction Innovations in Medical Education Wildlife Ecology and Conservation Molecular Biology Techniques and Applications Cancer Immunotherapy and Biomarkers Advanced Neural Network Applications Genomics and Phylogenetic Studies

Links

ORCID Lab Website Research Group UAMS TRI Profile

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OverviewAI-generated summary

Thomas J. Kelly is a Professor at the University of Arkansas for Medical Sciences with a distinguished research record, evidenced by an h-index of 90 and over 29,000 citations across 458 publications. His work has been recognized as high-impact, with recent publications spanning diverse areas including genomics, immunology, medical education, conservation biology, and cloning technology. Kelly leads a research group and maintains an active laboratory website, indicating ongoing research endeavors.

His collaborative network includes several researchers from the University of Arkansas for Medical Sciences, with whom he has co-authored multiple publications. These collaborators include Steven R. Post (6 shared publications), Bolni Marius Nagalo (4 shared publications), Martin J. Cannon (3 shared publications), and Camila Simões (3 shared publications). This indicates a collaborative approach to his research activities.

The breadth of Kelly's recent publications suggests engagement with multiple scientific disciplines. These include investigations into chromosome-specific telomere lengths using nanopore sequencing, the role of γδ intraepithelial lymphocytes in epithelial cell shedding, and the application of artificial intelligence in educational settings. Other publications address the impact of deforestation on extinction risk, industry perspectives on cloning timelines, predictors of CAR T-cell therapy neurotoxicity, and the repurposing of the MMR vaccine for cancer immunotherapy.

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: 458
Citations: 29,477

Selected Publications

Enhancing Neoadjuvant Virotherapy’s Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer (2024) DOI
<i>NR3C2</i> microdeletions—an underrecognized cause of pseudohypoaldosteronism type 1A: a case report and literature review (2024) DOI
The Tumor Microenvironment and Immune Response in Breast Cancer (2024) DOI
VT68.2: An Antibody to Chondroitin Sulfate Proteoglycan 4 (CSPG4) Displays Reactivity against a Tumor-Associated Carbohydrate Antigen (2023) DOI
Repurposing live attenuated trivalent MMR vaccine as cost-effective cancer immunotherapy (2022) DOI

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