Biography and Research Information
OverviewAI-generated summary
Tsung‐Jen Liao's research focuses on understanding the mechanisms and genetic factors contributing to drug-induced liver injury (DILI). His work investigates the role of UDP-Glucuronosyltransferase (UGT) enzymes in drug interactions that predict DILI and explores the impact of single-nucleotide polymorphisms (SNPs) as risk factors for chronic DILI, employing machine learning approaches for identification. Liao has also utilized whole exome sequencing to identify genetic variants, such as those in HLA class II genes, associated with transplant-free survival in acute liver failure, and variants in GBP4 that reduce risks for DILI in specific populations. His research extends to computational modeling for predicting drug and chemical hepatotoxicity and quantitative structure-activity relationship (QSAR) modeling for DILI prediction. Liao's scholarly contributions include 23 publications and 300 citations, with an h-index of 8. He collaborates with researchers at the National Center for Toxicological Research, including Minjun Chen, Baitang Ning, Kristin Ashby, and Tucker A. Patterson.
Metrics
- h-index: 8
- Publications: 23
- Citations: 300
Selected Publications
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Identification of Genetic Risk Factors Associated With Herbal and Dietary Supplement–Induced Acute Liver Failure Using Whole Exome Sequencing Analysis (2025)
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Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population (2025)
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Drug interaction with UDP-Glucuronosyltransferase (UGT) enzymes is a predictor of drug-induced liver injury (2024)
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Medical device report analyses from MAUDE: Device and patient outcomes, adverse events, and sex-based differential effects (2024)
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QSAR modeling for predicting drug-induced liver injury (2023)
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DILIrank dataset for QSAR modeling of drug-induced liver injury (2023)
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Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals (2023)
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Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure (2022)
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Machine Learning to Identify Interaction of Single-Nucleotide Polymorphisms as a Risk Factor for Chronic Drug-Induced Liver Injury (2021)
Collaboration Network
Top Collaborators
- Drug interaction with UDP-Glucuronosyltransferase (UGT) enzymes is a predictor of drug-induced liver injury
- Machine Learning to Identify Interaction of Single-Nucleotide Polymorphisms as a Risk Factor for Chronic Drug-Induced Liver Injury
- Medical device report analyses from MAUDE: Device and patient outcomes, adverse events, and sex-based differential effects
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
Showing 5 of 9 shared publications
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
- DILIrank dataset for QSAR modeling of drug-induced liver injury
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population
- Identification of Genetic Risk Factors Associated With Herbal and Dietary Supplement–Induced Acute Liver Failure Using Whole Exome Sequencing Analysis
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population
- Identification of Genetic Risk Factors Associated With Herbal and Dietary Supplement–Induced Acute Liver Failure Using Whole Exome Sequencing Analysis
- Machine Learning to Identify Interaction of Single-Nucleotide Polymorphisms as a Risk Factor for Chronic Drug-Induced Liver Injury
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
- DILIrank dataset for QSAR modeling of drug-induced liver injury
- DILIrank dataset for QSAR modeling of drug-induced liver injury
- Identification of Genetic Risk Factors Associated With Herbal and Dietary Supplement–Induced Acute Liver Failure Using Whole Exome Sequencing Analysis
- Genetic Variants of <i>GBP4</i>: Reduced Risks for Drug‐Induced Acute Liver Failure in Non‐Finnish European Population
- Identification of Genetic Risk Factors Associated With Herbal and Dietary Supplement–Induced Acute Liver Failure Using Whole Exome Sequencing Analysis
- Machine Learning to Identify Interaction of Single-Nucleotide Polymorphisms as a Risk Factor for Chronic Drug-Induced Liver Injury
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Whole Exome Sequencing Reveals Genetic Variants in HLA Class II Genes Associated With Transplant-free Survival of Indeterminate Acute Liver Failure
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
- Computational Modeling for the Prediction of Hepatotoxicity Caused by Drugs and Chemicals
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