Gunnar Boysen
Sourced from institutional research profiles (UAMS TRI or ARA).
Associate Professor -tenured
Also affiliated: University of Vermont (2007); University of North Carolina at Chapel Hill (2004–2025); National Institutes of Health (2006–2009); University of Minnesota (2003–2020); Lovelace Respiratory Research Institute (2007); Royal Marsden NHS Foundation Trust (2017); University of North Carolina Health Care (2008); University of Arizona (2020); Institute of Cancer Research (2017); Washington University in St. Louis (2020); University of Arkansas Medical Center (2009–2013); Cancer Institute (WIA) (2025); Center for Environmental Health (2007–2011); National Institute of Environmental Health Sciences (2006–2009); Winthrop Rockefeller Foundation (2011–2025); Conway School of Landscape Design (2020); Arkansas Department of Health (2013); UNC Lineberger Comprehensive Cancer Center (2007); Masonic Cancer Center (2003)
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Gunnar Boysen investigates the interactions between chemical exposures and nutritional or lifestyle factors, such as diet and physical activity, to understand their impact on human health. His research employs DNA and protein adducts as biomarkers to study carcinogen metabolism, how it is influenced by dietary components, and the underlying mechanisms that regulate enzyme activities involved in these processes.
Boysen's work also utilizes mass spectrometry-based metabolomic approaches, both targeted and untargeted, to investigate changes in common metabolic pathways resulting from environmental exposures. He has received federal funding from the NIH/National Institute of Environmental Health Sciences for his project "Understanding the origins of the mutational landscape in cancer," totaling $719,050. His scholarship metrics include an h-index of 33, 139 total publications, and 3,585 total citations. He leads a research group at the University of Arkansas for Medical Sciences and collaborates with several colleagues there, including Grover P. Miller, Azemat Jamshidi‐Parsian, Nadia I. Georgieva, and Intawat Nookaew.
Metrics
- h-index: 33
- Publications: 139
- Citations: 3,621
Selected Publications
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Abstract LB372: Understanding the origins of the mutational landscape (2026)
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Abstract 2326: Differentiating epigenetic marks and DNA adducts at the KRAS codon 12 mutation hotspot using ONT/ELIGOS sequencing (2026)
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Sex-Specific Formation of 1,2:3,4-Diepoxybutane-Derived Hemoglobin Adducts in 1,3-Butadiene-Exposed Workers (2025)
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Human health risk assessment for exposures to 1,3-butadiene in the United States with input from an independent science advisory panel (2025)
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Investigating the origins of the mutational signatures in cancer (2025)
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Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective <i>via</i> Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss (2024)
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CB-839 induces reversible dormancy in lung tumor-cells (2024)
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Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance (2023)
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Climate Change and New Challenges for Rural Communities: Particulate Matter Matters (2023)
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Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance (2023)
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Exploiting nanopore sequencing for characterization and grading of <i>IDH</i>‐mutant gliomas (2023)
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Similar 5F-APINACA Metabolism between CD-1 Mouse and Human Liver Microsomes Involves Different P450 Cytochromes (2022)
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Characterization of population variability of 1,3-butadiene derived protein adducts in humans and mice (2022)
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Nanopore Sequencing for Detection and Characterization of Phosphorothioate Modifications in Native DNA Sequences (2022)
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Current and Future Methodology for Quantitation and Site-Specific Mapping the Location of DNA Adducts (2022)
Federal Grants 1 $719,050 total
Understanding the origins of the mutational landscape in cancer
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Lipid Stress and MC4R (Funded by: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK))
- Cancer Prevention and Population Sciences Program UAMS College of Medicine
- ProfilingDoses of Reactive Compounds Derived from various Air Pollutant Exposures Environmental Protection Agency via The Health Effects Institute
- A novel approach for quantitation of N-terminal valine adducts NIH
- Arkansas Center for Clinical and Translational Research NIH
- The Role of N1-Inosine Adducts in Butadiene Mutagenesis NIH
- Systems Biology Based Diagnosis of Lung Cancer (Funded by: UAMS, Translational Research Institute (TRI))
- Monitoring Perfluoroalkyl and Polyfluoroalkyl Substances in Central Arkansas water systems US Department of Interior via University of Arkansas at Fayetteville
- Effects of Genetic Diversity on Carcinogen Metabolism NIH
- Mechanisms of Ethnic/Racial Differences in Lung Cancer Due to Cigarette Smoking NIH/Nat. Cancer Institute via University of Minnesota
- The Role of N1-Inosine Adducts in Butadiene Mutagenesis (Funded by: National Institute for Environmental Health Sciences (NIEHS))
Collaboration Network
Top Collaborators
- Impacts of diphenylamine NSAID halogenation on bioactivation risks
- CYP2C9 and 3A4 play opposing roles in bioactivation and detoxification of diphenylamine NSAIDs
- Bioactivation of Isoxazole-Containing Bromodomain and Extra-Terminal Domain (BET) Inhibitors
- Similar 5F-APINACA Metabolism between CD-1 Mouse and Human Liver Microsomes Involves Different P450 Cytochromes
- Structural Variations among Marketed Diphenylamine NSAIDs Determine Preference and Efficiency for Four Possible Bioactivation Pathways
- Impacts of diphenylamine NSAID halogenation on bioactivation risks
- CYP2C9 and 3A4 play opposing roles in bioactivation and detoxification of diphenylamine NSAIDs
- Bioactivation of Isoxazole-Containing Bromodomain and Extra-Terminal Domain (BET) Inhibitors
- Similar 5F-APINACA Metabolism between CD-1 Mouse and Human Liver Microsomes Involves Different P450 Cytochromes
- Structural Variations among Marketed Diphenylamine NSAIDs Determine Preference and Efficiency for Four Possible Bioactivation Pathways
- Current and Future Methodology for Quantitation and Site-Specific Mapping the Location of DNA Adducts
- Investigating the origins of the mutational signatures in cancer
- Exploiting nanopore sequencing for characterization and grading of <i>IDH</i>‐mutant gliomas
- Nanopore Sequencing for Detection and Characterization of Phosphorothioate Modifications in Native DNA Sequences
- Current and Future Methodology for Quantitation and Site-specific Mapping the Location of DNA Adducts
- Impacts of diphenylamine NSAID halogenation on bioactivation risks
- Bioactivation of Isoxazole-Containing Bromodomain and Extra-Terminal Domain (BET) Inhibitors
- Structural Variations among Marketed Diphenylamine NSAIDs Determine Preference and Efficiency for Four Possible Bioactivation Pathways
- Exploiting nanopore sequencing for characterization and grading of <i>IDH</i>‐mutant gliomas
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Impacts of diphenylamine NSAID halogenation on bioactivation risks
- Structural Variations among Marketed Diphenylamine NSAIDs Determine Preference and Efficiency for Four Possible Bioactivation Pathways
- Impacts of diphenylamine NSAID halogenation on bioactivation risks
- CYP2C9 and 3A4 play opposing roles in bioactivation and detoxification of diphenylamine NSAIDs
- CYP2C9 and 3A4 play opposing roles in bioactivation and detoxification of diphenylamine NSAIDs
- Similar 5F-APINACA Metabolism between CD-1 Mouse and Human Liver Microsomes Involves Different P450 Cytochromes
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
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