Igor P. Pogribny Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
◆ ARA Academy
High Impact
Researcher
faculty
76 h-index
295 pubs
18,020 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Igor P. Pogribny's research focuses on molecular toxicology and the epigenetic mechanisms underlying various diseases, particularly cancer. His work investigates the impact of environmental and occupational chemical carcinogens on genetic material and gene expression, with a significant emphasis on liver diseases like hepatocellular carcinoma and non-alcoholic fatty liver disease.
Pogribny utilizes animal models, including mice and rats, as well as model organisms like *Caenorhabditis elegans*, to assess the effects of chemical exposures and dietary interventions. His studies explore alterations in DNA methylation, gene expression, and telomerase activity, contributing to a deeper understanding of carcinogenesis and disease promotion. He has published extensively on these topics, with a substantial citation count and h-index, and is recognized as a highly cited researcher.
His research network includes several key collaborators from the National Center for Toxicological Research, including Volodymyr Tryndyak, Frederick A. Beland, Rose Willett, and Suresh K. Nagumalli, with whom he has co-authored numerous publications. Pogribny is also a member of the ARA Academy (ARA Fellow).
Metrics
- h-index: 76
- Publications: 295
- Citations: 18,020
Selected Publications
-
AMPK‐Dependent Epigenetic Regulation of Metabolism Mediates the Anti‐Cancer Action of Pterostilbene in Hepatocellular Carcinoma (2025)
-
Mediation analysis of the molecular phenotypes in a severe MASH-like liver injury mouse model (2025)
-
Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice (2025)
-
A preclinical model of severe NASH-like liver injury by chronic administration of a high-fat and high-sucrose diet in mice (2024)
-
Cellular and molecular alterations in a human hepatocellular in vitro model of nonalcoholic fatty liver disease development and stratification (2023)
-
Abstract 6017: Exposure-related DNA methylation and gene expression changes in mammary glands of Sprague Dawley rats treated with lorcaserin (2023)
-
Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice (2023)
-
Assessment of the effects of organic vs. inorganic arsenic and mercury in Caenorhabditis elegans (2022)
-
Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma (2022)
-
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)
-
Epigenetic changes induced in mice liver by methionine-supplemented and methionine-deficient diets (2022)
-
Erratum to: Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis (2021)
-
Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: An update of a systematic literature review (2021)
-
The DEN and CCl<sub>4</sub>‐Induced Mouse Model of Fibrosis and Inflammation‐Associated Hepatocellular Carcinoma (2021)
-
Supplementation of Choline-Deficient Diet With Pterostilbene Attenuates Cancer Development and Epigenetic Dysregulation of Gene Expression in Rat Livers (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
Volodymyr Tryndyak
National Center for Toxicological Research
31 shared publications
In database
- 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
- 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 31 shared publications
Aline de Conti
Centre international de recherche sur le cancer (FR)
27 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
Showing 5 of 27 shared publications
Frederick A. Beland
National Center for Toxicological Research
25 shared publications
In database
- 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
- 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 25 shared publications
Kostiantyn Dreval
Simon Fraser University (CA)
19 shared publications
- Signature gene expression model for quantitative evaluation of MASH-like liver injury in mice
- Table S1 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S3 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S6 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Table S2 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
Showing 5 of 19 shared publications
Orish Ebere Orisakwe
18 shared publications
- Table S1 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S3 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S6 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Table S2 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S2 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
Showing 5 of 18 shared publications
Sharon A. Ross
18 shared publications
- Table S1 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S3 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S6 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Table S2 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
- Figure S2 from Inhibition of the Cell Death Pathway in Nonalcoholic Steatohepatitis (NASH)-Related Hepatocarcinogenesis Is Associated with Histone H4 lysine 16 Deacetylation
Showing 5 of 18 shared publications
Ivan Rusyn
Texas A&M University (US)
8 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
- Effect of an obesogenic high-fat and high-sucrose diet on hepatic gene expression signatures in male Collaborative Cross mice
Showing 5 of 8 shared publications
Rose Willett
National Center for Toxicological Research
8 shared publications
In database
- 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
- 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
Mark Avigan
United States Food and Drug Administration (US)
5 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
- Lipidomic profiling of the hepatic esterified fatty acid composition in diet-induced nonalcoholic fatty liver disease in genetically diverse Collaborative Cross mice
- 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
Barbara Stefañska
University of British Columbia (CA)
4 shared publications
- 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
Cayla Boycott
University of British Columbia (CA)
4 shared publications
- 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
Megan Beetch
University of British Columbia (CA)
4 shared publications
- 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
Olga Kovalchuk
4 shared publications
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
Jody Filkowski
4 shared publications
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
James Meservy
4 shared publications
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Supplementary Table S1 from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
- Data from Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin
Similar Researchers
Based on overlapping research topics
Qingsu Xia
National Center for Toxicological Research
Carcinogens and Genotoxicity Assessment
Liver Disease Diagnosis and Treatment
Cancer-related molecular mechanisms research
Eric U. Yee
University of Arkansas for Medical Sciences
Liver Disease Diagnosis and Treatment
Metabolism and Genetic Disorders
Diet and metabolism studies
C D Collins
University of Arkansas for Medical Sciences
Liver Disease Diagnosis and Treatment
Cancer-related molecular mechanisms research
Metabolism and Genetic Disorders
Maria Theresa E. Montales
University of Arkansas for Medical Sciences
Liver Disease Diagnosis and Treatment
Cancer-related molecular mechanisms research
Metabolism and Genetic Disorders
Charles M. Skinner
University of Arkansas for Medical Sciences
Epigenetics and DNA Methylation
Carcinogens and Genotoxicity Assessment
Metabolism and Genetic Disorders
Ji‐Eun Seo
National Center for Toxicological Research
Carcinogens and Genotoxicity Assessment
Cancer-related molecular mechanisms research
Metabolism and Genetic Disorders