Igor P. Pogribny
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Researcher
Also affiliated: University of Lethbridge (2004–2010); University of North Carolina at Chapel Hill (2014); Louisiana State University (1999); Roswell Park Comprehensive Cancer Center (2008); Arkansas Children's Hospital (1999); Russian Academy of Sciences (2004); United States Food and Drug Administration (2004–2022); Heidelberg University (2004); Saginaw Valley State University (1999); Biochemical Society (2012–2015); Veterans Health Administration (2004); University Hospital Heidelberg (2004); Jackson Memorial Hospital (2008); In-Q-Tel (2010); Central Arkansas Veterans Healthcare System (2011); Texas A&M Health Science Center (2017); R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology (2008); Vavilov Institute of General Genetics (2004); Centre international de recherche sur le cancer (2018); The Ohio State University (2006); University of Tennessee at Knoxville (2006); Texas A&M University (2017)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Igor P. Pogribny's research focuses on the molecular mechanisms underlying chemical-induced toxicity and carcinogenesis, with a particular emphasis on epigenetic alterations. His work investigates how environmental and occupational chemical carcinogens impact DNA methylation, gene expression, and overall cellular processes. Pogribny has published extensively on these topics, with notable contributions to understanding the role of epigenetic changes in the development of liver diseases, including hepatocellular carcinoma and non-alcoholic fatty liver disease.
His laboratory utilizes various animal models, including mice and rats, as well as model organisms like *Caenorhabditis elegans*, to assess the effects of specific chemicals. Recent studies have explored the impact of dietary factors, such as methionine levels and structured lipids, on epigenetic modifications and carcinogenesis. Pogribny also examines the effects of heavy metals like arsenic and mercury on biological systems. His research is supported by a strong publication record, with a high h-index of 76 and over 18,000 citations, underscoring his significant contributions to the field of toxicology.
Metrics
- h-index: 76
- Publications: 293
- Citations: 18,121
Selected Publications
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AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma (2025)
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Mediation analysis of the molecular phenotypes in a severe MASH-like liver injury mouse model (2025)
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Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice (2025)
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A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice (2024)
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Cellular and molecular alterations in a human hepatocellular in vitro model of nonalcoholic fatty liver disease development and stratification (2023)
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Abstract 6017: Exposure-related DNA methylation and gene expression changes in mammary glands of Sprague Dawley rats treated with lorcaserin (2023)
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Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice (2023)
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Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice (2022)
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Assessment of the effects of organic vs. inorganic arsenic and mercury in Caenorhabditis elegans (2022)
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Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma (2022)
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Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet (2022)
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Epigenetic changes induced in mice liver by methionine-supplemented and methionine-deficient diets (2022)
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Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis (2021)
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Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: An update of a systematic literature review (2021)
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The DEN and CCl<sub>4</sub>‐Induced Mouse Model of Fibrosis and Inflammation‐Associated Hepatocellular Carcinoma (2021)
ARA Academy 2023 ARA Fellow
Dr. Pogribny is a distinguished scientist specializing in molecular toxicology and carcinogenesis. He earned his M.D. with honors from Ivano-Frankivsk National Medical University in Ukraine and a Ph.D. in Biochemistry/Oncology from Kyiv National Medical University. Since 2003, he has served as a research biologist and senior biomedical researcher at NCTR.
Policy Impact
Distinguished federal scientist at NCTR advancing understanding of chemical carcinogenesis, supporting the FDA's regulatory mission and public health protection from Arkansas.
Growth Areas
['Population Health Innovations & Clinical Research']
Resources
Collaboration Network
Top Collaborators
- Epigenetic changes induced in mice liver by methionine-supplemented and methionine-deficient diets
- Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
- A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice
- Cellular and molecular alterations in a human hepatocellular in vitro model of nonalcoholic fatty liver disease development and stratification
Showing 5 of 8 shared publications
- Assessment of the effects of organic vs. inorganic arsenic and mercury in Caenorhabditis elegans
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Epigenetic changes induced in mice liver by methionine-supplemented and methionine-deficient diets
- Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma
- AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma
Showing 5 of 7 shared publications
- The DEN and CCl<sub>4</sub>‐Induced Mouse Model of Fibrosis and Inflammation‐Associated Hepatocellular Carcinoma
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: An update of a systematic literature review
- Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
- A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice
Showing 5 of 7 shared publications
- Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
- A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice
- Cellular and molecular alterations in a human hepatocellular in vitro model of nonalcoholic fatty liver disease development and stratification
- Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice
Showing 5 of 7 shared publications
- Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
- A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice
- Cellular and molecular alterations in a human hepatocellular in vitro model of nonalcoholic fatty liver disease development and stratification
- Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice
Showing 5 of 6 shared publications
- Non-alcoholic fatty liver disease-associated DNA methylation and gene expression alterations in the livers of Collaborative Cross mice fed an obesogenic high-fat and high-sucrose diet
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
- A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice
- Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice
- Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma
- AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma
- Supplementation of Choline-Deficient Diet With Pterostilbene Attenuates Cancer Development and Epigenetic Dysregulation of Gene Expression in Rat Livers
- Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma
- AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma
- Supplementation of Choline-Deficient Diet With Pterostilbene Attenuates Cancer Development and Epigenetic Dysregulation of Gene Expression in Rat Livers
- Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma
- AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma
- Supplementation of Choline-Deficient Diet With Pterostilbene Attenuates Cancer Development and Epigenetic Dysregulation of Gene Expression in Rat Livers
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
- Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis
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