Robert L. Eoff
Professor
Also affiliated: Lutheran Medical Center (2024); California Lutheran University (2024); Vanderbilt University (2006–2011); University of Arkansas Medical Center (2017); Cancer Institute (WIA) (2025); Cancer Research Center (2008); Winthrop Rockefeller Foundation (2016–2025)
Faculty Researcher
Biochemistry & Molecular Biology, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Robert L. Eoff's research program focuses on understanding the fundamental mechanisms of DNA replication and repair, with a particular emphasis on their connection to human health and diseases such as cancer. His work utilizes a combination of biochemical and biophysical analyses, structural biology techniques including X-ray crystallography and molecular modeling, and mass spectrometry. Dr. Eoff has contributed to the Protein Data Bank with thirty-four crystal structure submissions, including five solved in his laboratory since joining the University of Arkansas for Medical Sciences (UAMS). He maintains an active collaboration with the Northeastern Collaborative Access Team (NE-CAT) at the Advanced Photon Source for X-ray data collection.
The research specifically investigates DNA damage tolerance pathways, aiming to elucidate their function under normal conditions and their dysregulation in tumorigenesis and aging. His laboratory has explored the role of specific polymerases, such as human polymerase ι, in the bypass of DNA lesions and the replication of challenging DNA structures like G-quadruplexes. Recent publications from his group address the inhibition of invasion in glioblastoma using organoid models, the activity of natural compounds against cancer, and the role of specific enzymes in DNA damage tolerance and repair within glioma cells.
Dr. Eoff is a high-impact researcher with an h-index of 30 and has secured significant federal funding, including a $2.295 million NIH grant for the Center for Molecular Interactions in Cancer (CMIC) and a $1.1 million NSF grant for research on G-quadruplex DNA replication by translesion polymerases. He actively collaborates with colleagues at UAMS, including Megan R. Reed, Amit Ketkar, Analiz Rodriguez, and Leena Maddukuri.
Research Overview
The research I pursue is focused on DNA replication and seeks to provide fundamental insights into how these mechanisms are related to human health, especially cancer. I have expertise in a number of areas pertinent to the current application including: biochemical/biophysical analysis of enzymes, structural biology (X-ray crystallography and molecular modeling techniques), mass spectrometry and genomic instability in cancer. In addition to in silico modeling approaches, I have been involved in solving thirty-four crystal structures submitted to the Protein Data Bank. I am first author on seventeen of these PDB submissions, and my laboratory has solved five crystal structures since I joined the faculty at UAMS. I have an active collaboration (General users proposal, GUP-41183) with the Northeastern collaborative access team (NE-CAT) at the Advanced Photon Source (APS) that grants us access to the 24-ID-E and 24-ID-C beamlines for data collection. The research I pursue is focused on DNA damage tolerance pathways and seeks to provide fundamental insights into how these mechanisms function under basal conditions and how they go astray during tumorigenesis or as a function of age. I have received funding from the National Institutes of Health in the form of an R00 award (GM084460) and a R01 (CA183895). I have established a strong research program with two senior post-doctoral fellows and three Ph.D. students. In less than four years, my team has published nine full, peer-reviewed research articles on which I am corresponding author. Work from my group has recently culminated in a manuscript that reveals important and previously unrecognized properties related to Werner’s syndrome protein (WRN) modulation of polymerase activity during bypass of oxidative DNA damage. Experiments from my group illustrate that WRN has a strong impact on the DNA adduct bypass properties of human DNA polymerases (pols) eta and kappa, inducing more accurate synthesis across oxidative damage (published in The Journal of Biological Chemistry and Nucleic Acids Research). Another study from my laboratory that was conducted in collaboration with Prof. Peter Crooks (UAMS) identified novel small-molecule inhibitors of the replication stress response enzyme human DNA polymerase eta, with the resulting manuscript recently being published in ACS Chemical Biology. We continue to pursue projects related to translesion polymerase activity in cancer and are actively developing new TLS pol inhibitors as a way to sensitize tumors to genotoxic anti-cancer drugs (e.g. cisplatin, doxorubicin). My long-term goal is to contribute in a meaningful fashion to the scientific endeavors that seek to improve human health, our ability to treat disease & our fundamental understanding of living systems.
Metrics
- h-index: 31
- Publications: 118
- Citations: 2,721
Selected Publications
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Human REV1 interacts with DHX36 to promote replication and tolerance of G-quadruplex DNA (2026)
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Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models (2025)
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Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model (2025)
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Abstract 1488: DNA polymerase kappa slows replication fork speed by promoting fork reversal in glioblastoma (2025)
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Abstract 1333 DNA polymerase kappa (Pol k) promotes replication gap suppression by preventing PrimPol mediated repriming and safeguards genomic stability in Glioblastoma Multiforme (GBM) (2024)
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Conservation of the insert-2 motif confers Rev1 from different species with an ability to disrupt G-quadruplexes and stimulate translesion DNA synthesis (2023)
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Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer (2022)
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Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer (2022)
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323 Generation of a functional precision medicine pipeline which combines comparative transcriptomics and tumor organoid modeling to identify bespoke treatment strategies for glioblastoma (2022)
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Site-Specific Synthesis of Oligonucleotides Containing 6-Oxo-M<sub>1</sub>dG, the Genomic Metabolite of M<sub>1</sub>dG, and Liquid Chromatography–Tandem Mass Spectrometry Analysis of Its In Vitro Bypass by Human Polymerase ι (2021)
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A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma (2021)
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Biobanked Glioblastoma Patient-Derived Organoids as a Precision Medicine Model to Study Inhibition of Invasion (2021)
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Inositol serves as a natural inhibitor of mitochondrial fission by directly targeting AMPK (2021)
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Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models (2021)
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Deletion of putative xenobiotic response elements (XREs) in hpol κ alters the replication stress response and overall genomic instability in glioblastoma cells (2021)
Federal Grants 2 $3,395,000 total
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Advancing Breast Cancer Treatment through Suppression of Chemo-Resistance UAMS Executive Breast Committee Principal Investigator
- Functions and Mechanisms of Helicases and G-Quadruplex Nucleic Acids NIH Co-Investigator
- Coordinating Translesion DNA Synthesis Opposite Damaged DNA NIH Principal Investigator
- ABI R. Eoff COBRE FY26 Y2 State of Arkansas Principal Investigator
- Seeds of Science Pilot award UAMS Internal Research Awards Principal Investigator
- Translesion DNA polymerase kappa activity in gliomas NIH Principal Investigator
- Translesion Synthesis Opposite Carcinogen Bound DNA NIH Principal Investigator
- Mechanistic characterization of the cell cycle-dependent DNA repair pathway- Resubmission NIH/Nat. Cancer Institute Principal Investigator
- G-quadruplex DNA as a chemical signaling agent NIH Co-Investigator
Collaboration Network
Top Collaborators
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
Showing 5 of 15 shared publications
- Inositol serves as a natural inhibitor of mitochondrial fission by directly targeting AMPK
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- Site-Specific Synthesis of Oligonucleotides Containing 6-Oxo-M<sub>1</sub>dG, the Genomic Metabolite of M<sub>1</sub>dG, and Liquid Chromatography–Tandem Mass Spectrometry Analysis of Its In Vitro Bypass by Human Polymerase ι
- Conservation of the insert-2 motif confers Rev1 from different species with an ability to disrupt G-quadruplexes and stimulate translesion DNA synthesis
Showing 5 of 8 shared publications
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
Showing 5 of 6 shared publications
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
- Abstract PS18-46: Inhibition of breast cancer stem cells in 2- and 3-dimensional culture by novel salinomycin analogs
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
Showing 5 of 6 shared publications
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
- Abstract PS18-46: Inhibition of breast cancer stem cells in 2- and 3-dimensional culture by novel salinomycin analogs
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
Showing 5 of 6 shared publications
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
- Abstract PS18-46: Inhibition of breast cancer stem cells in 2- and 3-dimensional culture by novel salinomycin analogs
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
Showing 5 of 6 shared publications
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
- Abstract PS18-46: Inhibition of breast cancer stem cells in 2- and 3-dimensional culture by novel salinomycin analogs
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
Showing 5 of 6 shared publications
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- Biobanked Glioblastoma Patient-Derived Organoids as a Precision Medicine Model to Study Inhibition of Invasion
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- 323 Generation of a functional precision medicine pipeline which combines comparative transcriptomics and tumor organoid modeling to identify bespoke treatment strategies for glioblastoma
Showing 5 of 6 shared publications
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Deletion of putative xenobiotic response elements (XREs) in hpol κ alters the replication stress response and overall genomic instability in glioblastoma cells
- Single and double modified salinomycin analogs target stem-like cells in 2D and 3D breast cancer models
- Abstract PS18-46: Inhibition of breast cancer stem cells in 2- and 3-dimensional culture by novel salinomycin analogs
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer
- Monensin and its analogues show anti‐glioblastoma activity in an organoid model of cancer
- Monensin and Its Analogs Exhibit Activity Against Breast Cancer Stem-Like Cells in an Organoid Model
- Evaluation of the Activity of Monensin and Its Analogs for Modulation of Stem-like Cell Functionality in 2D and 3D Breast Cancer Models
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